Loading...

A.O.C 5.1 & 5.2 review
Quiz by Joseph Mibb
Customize this quiz to suit your class
Instantly translate to 100+ languages
Tag the questions with any skills you have. Your dashboard will track each student's mastery of each skill.
Give this quiz to my class
Lipids are large, nonpolar organic molecules. They do not dissolve in water. Lipids include triglycerides (trie-GLIS-uhr-IEDZ), phospho- lipids, steroids, waxes, and pigments. Lipid molecules have a higher ratio of carbon and hydrogen atoms to oxygen atoms than carbohydrates have. Because lipid molecules have larger numbers of carbon-hydrogen bonds per gram than other organic com- pounds do, they store more energy per gram. Fatty Acids Fatty acids are unbranched carbon chains that make up most lipids. Figure 3-10 shows that a fatty acid contains a long carbon chain (from 12 to 28 carbons) with a carboxyl group, —COOH, attached at one end. The two ends of the fatty-acid molecule have different properties. The carboxyl end is polar and is thus hydrophilic or attracted to water molecules. In contrast, the hydro- carbon end of the fatty-acid molecule is nonpolar. This end tends not to interact with water molecules and is said to be hydrophobic (HIE-droh-FOH-bik), or “water fearing.” In saturated fatty acids, such as palmitic acid, which is shown in Figure 3-10, each carbon atom is covalently bonded to four atoms. The carbon atoms are in effect full, or saturated. In contrast, linoleic acid, also shown in Figure 3-10, has carbon atoms that are not bonded to the maximum number of atoms to which they can bond. Instead, they have formed double bonds within the carbon chain. This type of fatty acid is said to be unsaturated. Triglycerides Three classes of lipids important to living things contain fatty acids: triglycerides (fats), phospholipids, and waxes. A triglyceride is composed of three molecules of fatty acid joined to one molecule of the alcohol glycerol. Saturated triglycerides are composed of saturated fatty acids. They typically have high melting points and tend to be hard at room temperature. Common dietary saturated triglycerides include butter and fats in red meat. In contrast, unsaturated triglycerides are composed of unsaturated fatty acids and are usually soft or liquid at room temperature. Unsaturated triglycerides are found primarily in plant seeds where they serve as an energy and carbon source for germinating plants. Phospholipids Phospholipids have two, rather than three, fatty acids attached to a molecule of glycerol. They have a phosphate group attached to the third carbon of the glycerol. As shown in Figure 3-11, the cell membrane is made of two layers of phospholipids, called the lipid bilayer. The inability of lipids to dissolve in water allows the mem- brane to form a barrier between the inside and outside of the cell. Hydrophilic “head” Phospholipids Hydrophobic “tail” Phospholipids Water Water The lipid bilayer of a cell membrane is a double row of phospholipids.The “tails” face each other.The “head” of a phospholipid, which contains a phosphate group, is polar and hydrophilic.The two tails are two fatty acids and are nonpolar and hydrophobic. FIGURE 3-11 H C H C O OH H C H H C H H C H H C H H C H H C H H C H H C H H C H H C H H C H H C H C H H H H C H H C H H C H H C H H C H C O OH H C H H C H H C H C H C H C H H C H H C H C H H C H H C H C H H H H C H Fatty acids have a polar carboxyl head, highlighted in purple, and a nonpolar hydrocarbon tail, highlighted in green. FIGURE 3-10 Palmitic acid Linoleic acid mb06se_bchs02.qxd 5/18/07 10:49 AM Page 59 60 CHAPTER 3 1. Compare the structure of monosaccharides, dis- accharides, and polysaccharides. 2. How are proteins constructed from amino acids? 3. How do amino acids differ from one another? 4. Describe a model of enzyme action. 5. Why do phospholipids orient in a bilayer when in a watery environment, such as a cell? 6. Describe how the three major types of lipids differ in structure from one another. 7. What are the functions of the two types of nucleic acids? CRITICAL THINKING 8. Applying Information Before a long race, run- ners often “carbo load.” This means that they eat substantial quantities of carbohydrates. How might this help their performance? 9. Recognizing Relationships High temperatures can weaken bonds within a protein molecule. How might this explain the effects of using a hot curling iron or rollers in one’s hair? 10. Applying Information You want to eat more unsaturated than saturated fats. Name examples of foods you would eat more of and less of. SECTION 2 REVIEW Waxes A wax is a type of structural lipid consisting of a long fatty-acid chain joined to a long alcohol chain. Waxes are waterproof, and in plants, form a protective coating on the outer surfaces. Waxes also form protective layers in animals. For example, earwax helps pre- vent microorganisms from entering the ear canal. Steroids Unlike most other lipids, which are composed of fatty acids, steroid molecules are composed of four fused carbon rings with various functional groups attached to them. Many animal hor- mones, such as the male hormone testosterone, are steroid com- pounds. One of the most familiar steroids in humans is cholesterol. Cholesterol is needed by the body for nerve and other cells to func- tion normally. It is also a component of the cell membrane. NUCLEIC ACIDS Nucleic acids are very large and complex organic molecules that store and transfer important information in the cell. There are two major types of nucleic acids: deoxyribonucleic acid and ribonucleic acid. Deoxyribonucleic acid, or DNA, contains information that deter- mines the characteristics of an organism and directs its cell activi- ties. Ribonucleic (RIE-boh-noo-KLEE-ik) acid, or RNA, stores and transfers information from DNA that is essential for the manufactur- ing of proteins. Some RNA molecules can also act as enzymes. Both DNA and RNA are polymers, composed of thousands of linked monomers called nucleotides (NOO-klee-uh-TIEDS). As shown in Figure 3- 12, each nucleotide is made of three main components: a phosphate group, a five-carbon sugar, and a ring-shaped nitrogenous base.
Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty Desirée Nieuwenhuis | Natàlia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. Dif- ferential role of adipose tissues in obesity and related metabolic and vas- cular complications. 2016;2016:1-15, 1216783. 6. Zwick RK, Guerrero-Juarez CF, Horsley V, Plikus MV. Anatomical, physiological, and functional diversity of adipose tissue. Cell Metab. 2018;27(1):68-83. 7. Gulyaeva O, Dempersmier J, Sul HS. Genetic and epigenetic control of adipose development. Biochimica et Biophysica Acta (BBA)— Molecular and Cell Biology of Lipids. 2019;1864:3-12. 8. Khan M, Joseph F. Adipose tissue and adipokines: the association with and application of adipokines in obesity. Forensic Sci. 2014;2014: 711-724, 328592. 9. Alotaibi MF. Physiology of puberty in boys and girls and pathological disorders affecting its onset. J Adolesc. 2019;71:63-71. 10. Cousminer DL, Stergiakouli E, Berry DJ, et al. Genome-wide associa- tion study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty. Hum Mol Genet. 2014;23(16):4452-4464. 11. Ahmed ML, Ong KK, Dunger DB. Childhood obesity and the timing of puberty. Trends in endocrinology and metabolism: TEM. 2009;20(5): 237-242. 12. Biro FM, Pajak A, Wolff MS, et al. Age of menarche in a longitudinal US cohort. J Pediatr Adolesc Gynecol. 2018;31(4):339-345. 13. Currie C, Ahluwalia N, Godeau E, Nic Gabhainn S, Due P, Currie DB. Is obesity at individual and national level associated with lower age at menarche? Evidence from 34 countries in the Health Behaviour in School-aged Children Study. The Journal of adolescent health: official publication of the Society for Adolescent Medicine. 2012;50(6): 621-626. 14. De Leonibus C, Marcovecchio ML, Chiavaroli V, de Giorgis T, Chiarelli F, Mohn A. Timing of puberty and physical growth in obese children: a longitudinal study in boys and girls. Pediatr Obes. 2014; 9(4):292-299. 15. Flom JD, Cohn BA, Tehranifar P, et al. Earlier age at menarche in girls with rapid early life growth: cohort and within sibling analyses. Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, Widén E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999–2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, Schönbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. Böttner A, Jr K, Müller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, Iñiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. Corrigendum to: Increased high molecular weight adiponectin, but decreased total adiponectin and kisspeptin, in central precocious puberty compared with aged-matched prepubertal girls. Reprod Fertil Dev. 2017;29:2506-2517. 64. Das UN. Is obesity an inflammatory condition? Nutrition. 2001; 17(11-12):953-966. 65. Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Hum Reprod Update. 2014; 20(2):153-174. 66. Singh A, Choubey M, Bora P, Krishna A. Adiponectin and chemerin: contrary adipokines in regulating reproduction and metabolic disor- ders. Reproductive sciences (Thousand Oaks, Calif). 2018;25:1462- 1473. 67. Tsatsanis C, Dermitzaki E, Avgoustinaki P, Malliaraki N, Mytaras V, Margioris AN. The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis. Hormones (Athens). 2015; 14:549-562. 68. Kang MJ, Oh YJ, Shim YS, Baek JW, Yang S. Hwang IT. The usefulness of circulating levels of leptin, kisspeptin, and neurokinin B in obese girls with precocious puberty. 2018;34:627-630. 69. Lee J, Song J, Hootman JM, et al. Obesity and other modifiable fac- tors for physical inactivity measured by accelerometer in adults with knee osteoarthritis: data from the osteoarthritis initiative (OAI). Arthritis Care Res (Hoboken). 2012;53-61. 70. Bramswig J, Dubbers A. Disorders of pubertal development. Deutsches Arzteblatt international. 2009;106:295-303. quiz 04 71. Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertil- ity. Cell Mol Life Sci. 2013;70(5):841-862. 72. Riumallo J, Durnin JV. Changes in body composition in adolescent boys. Eur J Clin Nutr. 1988;42(2):107-112. 73. Siervogel RM, Demerath EW, Schubert C, et al. Puberty and body composition. Horm Res. 2003;60(Suppl 1):36-45. 74. Zhang J. Gong M. Andrologia: Review of the role of leptin in the regu- lation of male reproductive function; 2018. 75. Kauffman AS, Gottsch ML, Roa J, et al. Sexual differentiation of Kiss1 gene expression in the brain of the rat. Endocrinology. 2007;148(4): 1774-1783. 76. Zeydabadi Nejad S, Ramezani Tehrani F, Zadeh-Vakili A. The role of kisspeptin in female reproduction. Int J Endocrinol Metab. 2017;15:1- 11, e44337. 77. Sorensen K, Aksglaede L, Petersen JH, Juul A. Recent changes in pubertal timing in healthy Danish boys: associations with body mass index. J Clin Endocrinol Metab. 2010;95(1):263-270. 78. Juul A, Magnusdottir S, Scheike T, Prytz S, Skakkebaek NE. Age at voice break in Danish boys: effects of pre-pubertal body mass index and secular trend. Int J Androl. 2007;30(6):537-542. 79. Lee JM, Wasserman R, Kaciroti N, et al. Timing of puberty in overweight versus obese boys. Pediatrics. 2016;137(2):137-146, e20150164. 80. He F, Guan P, Liu Q, Crabtree D, Peng L, Wang H. The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. Secondary sexual characteristics in boys: data from the Pediatric Research in Office Settings Network. Pediatrics. 2012;130(5):e1058-e1068. 86. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452. 87. Akin I, Tolg R, Hochadel M, et al. No evidence of “obesity paradox” after treatment with drug-eluting stents in a routine clinical practice: results from the prospective multicenter German DES.DE (German Drug-Eluting Stent) Registry. JACC Cardiovasc Interv. 2012;5(2): 162-169. 88. Marcovecchio ML, Chiarelli F. Obesity and growth during childhood and puberty. World Rev Nutr Diet. 2013;106:135-141. How to cite this article: Nieuwenhuis D, Pujol-Gualdo N, Arnoldussen IAC, Kiliaan AJ. Adipokines: A gear shift in puberty. Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are gover
A solution is composed of a solute dissolved in a solvent. In the sugar water described in Figure 5-1, the solute was sugar and the solvent was water, and the solute molecules diffused through the solvent. It is also possible for solvent molecules to diffuse. In the case of cells, the solutes are organic and inorganic compounds, and the solvent is water. The process by which water molecules diffuse across a cell membrane from an area of higher concentration to an area of lower concentration is called osmosis (ahs-MOH-sis). Because water is moving from a higher to lower concentration, osmosis does not require cells to expend energy. Therefore, osmosis is the passive transport of water. Direction of Osmosis The net direction of osmosis depends on the relative concentra- tion of solutes on the two sides of the membrane. Examine Table 5-1. When the concentration of solute molecules outside the cell is lower than the concentration in the cytosol, the solution outside is hypotonic to the cytosol. In this situation, water diffuses into the cell until equilibrium is established. When the concentration of solute molecules outside the cell is higher than the concentration in the cytosol, the solution outside is hypertonic to the cytosol. In this situation, water diffuses out of the cell until equilibrium is established. Observing Diffusion Materials 600 mL beaker, 25 cm dialysis tubing, funnel, 15 mL starch solution (10 percent), 20 drops Lugol’s solution, 300 mL water, 100 mL graduated cylinder, 20 cm piece of string (2) Procedure 1. Put on your disposable gloves, lab apron, and safety goggles. 2. Pour 300 mL of water in the 600 mL beaker. 3. Add 20 drops of Lugol’s solution to the water. CAUTION: Lugol’s solution is a poison and eye and skin irritant. 4. Open the dialysis tubing, and tie one end tightly with a piece of string. 5. Using the funnel, pour 15 mL of 10 percent starch solution into the dialysis tubing. 6. Tie the other end of the dialysis tubing tightly with the second piece of string, forming a sealed bag around the starch solution. 7. Place the bag into the solution in the beaker, and observe the setup for a color change. Analysis What happened to the color in the bag? What happened to the color of the water around the bag? Explain your observations. Quick Lab www.scilinks.org Topic: Osmosis Keyword: HM61090 mb06se_homs01.qxd 11/27/07 8:52 AM Page 98 HOMEOSTASIS AND CELL TRANSPORT 99 When the concentrations of solutes outside and inside the cell are equal, the outside solution is said to be isotonic to the cytosol. Under these conditions, water diffuses into and out of the cell at equal rates, so there is no net movement of water. Notice that the prefixes hypo-, hyper-, and iso- refer to the relative solute concentrations of two solutions. Thus, if the solution outside the cell is hypotonic to the cytosol, then the cytosol must be hyper- tonic to that solution. Conversely, if the solution outside is hypertonic to the cytosol, then the cytosol must be hypotonic to the solution. Water tends to diffuse from hypo- tonic solutions to hypertonic solutions. How Cells Deal with Osmosis Cells that are exposed to an isotonic external environment usually have no difficulty keeping the movement of water across the cell membrane in balance. This is the case with the cells of ver- tebrate animals on land and of most other organ- isms living in the sea. In contrast, many cells function in a hypotonic environment. Such is the case for unicellular freshwater organisms. Water constantly diffuses into these organisms. Because they require a relatively lower concentration of water in the cytosol to function normally, unicel- lular organisms must rid themselves of the excess water that enters by osmosis. Some of them, such as the paramecia shown in Figure 5-2, do this with contractile vacuoles (kon-TRAK-til VAK-y ̄ ̄o ̄ ̄o-OL), which are organelles that remove water. Contractile vacuoles collect the excess water and then contract, pumping the water out of the cell. Unlike diffusion and osmosis, this pumping action is not a form of passive trans- port because it requires the cell to expend energy. Copyright © by Holt, Rinehart and Winston. All rights reserved. (a) (b) Vacuole filling with water Vacuole contracting TABLE 5-1 Direction of Osmosis Condition External solution is hypotonic to cytosol External solution is hypertonic to cytosol External solution is isotonic to cytosol Net movement of water into the cell out of the cell none H2O H2O H2O H2O H2O H2O The paramecia shown below live in fresh water, which is hypotonic to their cytosol. (a) Contractile vacuoles collect excess water that moves by osmosis into the cytosol. (b) The vacuoles then contract, returning the water to the outside of the cell. (LM 315) FIGURE 5-2 100 CHAPTER 5 (a) HYPOTONIC Cell walls (b) HYPERTONIC (a) ISOTONIC (b) HYPOTONIC (c) HYPERTONIC Other cells, including many of those in multicellular organisms, respond to hypotonic environments by pumping solutes out of the cytosol. This lowers the solute concentration in the cytosol, bring- ing it closer to the solute concentration in the environment. As a result, water molecules are less likely to diffuse into the cell. Most plant cells, like animal cells, live in a hypotonic environ- ment. In fact, the cells that make up plant roots may be surrounded by water. This water moves into plant cells by osmosis. These cells swell as they fill with water until the cell membrane is pressed against the inside of the cell wall, as Figure 5-3a shows. The cell wall is strong enough to resist the pressure exerted by the water inside the expanding cell. The pressure that water molecules exert against the cell wall is called turgor pressure (TER-GOR PRESH-er). In a hypertonic environment, water leaves the cells through osmosis. As shown in Figure 5-3b, the cells shrink away from the cell walls, and turgor pressure is lost. This condition is called plasmolysis (plaz-MAHL-uh-sis), and is the reason that plants wilt if they don’t receive enough water. Some cells cannot compensate for changes in the solute con-
Make mcq quiz with 4 option in which one is correct -'10 Basis of Material Science • .....;;;";;;"~~;;,,;;,,,,;.;.,,;;,,,;,,;.;,.,------------ 6. Temporary materials: Some materials are meant to be placed in the oral cavity for a short period of time for different reasons. • Temporary crowns: While a permanent crown is prepared in the dental laboratory, the patient must wait for few days before it can be fabricated and cemented into place. Does patient experience any problems during this time period? If the tooth is vital (the pulp is alive), the patient is likely to experience pain and sensitivity while eating and drinking, also it looks unesthetic. What can be done to solve this problem? A temporary crown is placed before the patient leaves the clinic. It is constructed and luted in the same appointment in which the crown preparation is done. Temporary crowns are not very strong or esthetic but they serve adequately till the permanent crown is ready to be cemented. • Temporary restorations: Sometimes it is difficult to decide immediately the best line of treatment for a particular tooth. The exact condition of the pulp may not be obvious to the dentist from the patient's symptoms. A dentist removes all or part of the decay and then places a temporary restoration to have time to observe the behaviour of the pulp or to give the pilip time to heal before deciding the further treatment required. Classification based on Location of Fabrication 4,9 Materials can be classified based on the location of fabrication into: • Direct restorative materials. • Indirect restorative materials Direct restorative materials: They include those materials which are used to restore cavity preparations directly in the oral cavity (Box 1.5). Box 1.5: Examples of direct restorative materials Amalgam, composites, glass ionomer and other materials, which set by chemical reactions in the mouth. Indirect restorative materials: It includes those restorations which must be fabricated outside the mouth, indirectly on a cast/ model/ die, because their processing condition would harm oral tissues. Materials used in the construction of such prosthesis are called indirect restorative materials (Box 1.6). Box 1.6: Examples of indirect restorative materials Gold inlays, crowns of metal, ceramic and polymers, which are processed at elevated temperatures. Some indirect composite restorations can be processed under specific wavelength of light, e.g. Ceramage. Classification based on Longevity of Use 1. Permanent restorations: These restorations are not planned to be replaced for a particular time period. Though they are referred to as permanent, actually they are not, e.g. fillings, crowns, bridges and dentures do not last forever (Fig. 1.5). 2. Temporary restorations: These restorations are planned to be replaced in a short period of time, such as few days to weeks. For ~ Permanent C/) c c -.2 0 c- :;::; Cll co Interim ~ Q; 0 .8ll::1iJ C/) o~ Cll a:: c:=:J Temporary Time period Fig. 1.5: Diagram depicting the time period of use of a restoration. (Arrow in permanent restoration depicts that such restorations are not planned to be replaced for a long period of time.) Introducton to Dental Materials Dental materials Box 1.7: Characteristics of metals 1. High thermal and electrical conductivity 2. Ductility (pure metals are very soft and they can be bent without breaking) 3. Opacity (they do not transmit light) 4. Luster (they have a surface that strongly reflects light and appears bright and shiny) 5. They tend to dissolve to some extent in water or other aqueous solutions, producing cations. 6. All metals are white (actually gray) except for gold, which is yellow, and copper, which is reddish. 7. All metals are solid at room temperature except mercury, which is liquid at room temperature and is used with silver alloys as amalgam. 8. All metals have high melting temperatures because of high strength of the metallic bond that holds the atoms together. 3. Polymers 4. Composites Composites are mixtures of two or more of the first three classes in which the different components remain distinct from one another in the final structure. A common example is composite resin. Fig. 1.7a: Three-dimensional structure of iron (metal) Metals Metals are the oldest of the three classes of materials that have been used as dental materials. Metals are characterized by metallic bonds (Box 1.7) which will be discussed in the next chapter. Metals solidify with their atoms in a regular or crystalline arrangement (see Chapter 2), often in the form of a cube (Fig. 1.7a). example, temporary fillings done in a tooth during root canal treatment, which have to be replaced within 2-4 days during subsequent visits. They are used to protect the tooth and provide function till the final restoration is done. 3. Interim restoration: At times, dental treatment requires "long-term" definite temporary restorations or "interim" restorations. For examle, a 7-year-old child, met with trauma and fractured one of his central incisors. A large composite build- up may serve his immediate requirement until the root formation is completed and a permanent crown is placed. 5 Classification based on the Chemical Nature of the Material These are the atoms that make up a material and the way they are bonded together determine the properties of that materiaLS Weak bonds make for weak materials and vice versa (Table 1.4). Materials can be classified into different categories based on their primary atomic bonds (Fig. 1.6): 1. Metals 2. Ceramics Fig. 1.6: Classification of dental materials based on chemical nature 12 Basis of Material Science Box 1.9: Benefits of ceramics in dentistry 1. Many ceramic oxides are used as pigmenting agents. These oxides produce good range of colors. Due to this characteristic, we are able to match almost any tooth color with good esthetic results. 2. They are inert, i.e. not chemically reactive. This quality provides ceramics with good bio- compatibility. 3. Ceramic materials are translucent, like natural teeth. This translucency gives the ceramic crown a more natural appearance than any other dental material. Fig. 1.7b: Internal arrangement of tetrahedral structure of ceramic (silica) four large oxygen atoms surround smaller silicon atom Ceramics A ceramic is a compound formed by the union of a metallic and a non-metallic element (Box 1.8). Most of these materials are oxides, formed by the union of oxygen with metals such as silicon, aluminum, calcium and magnesium (Fig.1.7b). Ceramics may be simple or complex. Examples of simple ceramics are alumina and silica. Examples of complex ceramics are feldspar (potassium aluminum silicate) and kaolin (hydrated aluminum silicate). Ceramics may be crystalline or non- crystalline (i.e. amorphous). Porcelain is a specific type of ceramic used extensively in dentistry (Box 1.9). Box 1.8: Characteristics of ceramics 1. High melting points. 2. Brittleness, which means they cannot be bent or deformed (no sliding) to any extent without actually cracking and breaking. 3. They are poor conductor of heat and electricity. 4. They are chemically inert. 5. They have excellent esthetic result in terms of matching natural teeth. Fig. 1.8: Stucture of synthetic polymer Polymers They are the latest addition (early to mid- 1900s) to dental materials. Most of the polymers are nowadays synthesized by humans. Polymers are giant, long-chain organic molecules (Fig. 1.8). Polymers are characterized by covalent bonds within each molecule, giving them tremendous strength in a single direction. Try to break a nylon rope by pulling it! They are poor conductors of heat and electri- city. Most polymers have a structure containing thousands of carbon atoms linked together like beads on a string. Others, such as silicone polymers are formed with silicon-oxygen bonds. Introducton to Dental Materials Table 1.4: Characteristics of different materials 13 Characteristics Bond Properties Crystal structure Metals Metallic bonding High strength and hardness, high electrical and thermal conductivity BCC, FCC, or HCP unit cells Ceramics Ionic or covalent bonding, or both High hardness and stiffness, electrically insulating, refractory, and chemically inert Crystalline or amorphous Polymers Covalent bonding Low sensitivity, high electrical resistivity, and low thermal conductivity, strength and stiffness vary widely Amorphous and crystalline Composites Composites are combinations of any of the basic ceramic, metallic and polymeric materials (Box 1.10). Each material that makes up composites is called a phase. Their properties tend to be somewhere between those of their basic constituents and are used to enhance their performance, longevity and handling chracterstics. Box 1.10: Types of composites in dentistry 1. Ceramic - metallic composite: Tungsten carbide bur. 2. Metal - polymer composite: Die materials in dental laboratory. 3. Ceramic - polymer composite: Enamel, dentin, bone and restorative composites. A composite is a kind of "combination" of materials, which compliment each other. The properties lacking in one material are compensated by those of the other material. For example, restorative composite has two phases, namely resin and fillers. Teeth and bones are examples of natural composites. Enamel is a composite of hydroxyapatite (which is a ceramic material) and protein (which is a polymer). EVALUATION OF DENTAL MATERIALS Most manufacturers of dental materials maintain a quality assurance programme (As per international standard like ADA specifications) and materials are thoroughly tested before being released into the market for dental practitioner (Fig. 1.9). Laboratory Evaluations Most ADA/ ANSI specifications involve laboratory tests. The tests performed as per these specifications are useful but they all are performed in vitro, (carried out in the laboratory away from the clinical conditions) which have a lot of limitations in clinical practice.lO Clinical Notes 1. For example, most of the direct restorative materials are tested for their compressive strength but ultimately the material is subjected to a combination of compressive, tensile and shear stresses, which may decide the final success or failure of the material under masticatory load. 2. Similarly upper dentures mostly fracture along the midline because of bending. Hence a bending or transverse strength ~B-a-s-is-o-f-M-a-t-e-ria-I-S~c-ie-n-c-e-------------- ---------. test is far more meaningful for denture base materials than a compression test. Clinical Trials The majority of new materials are subjected to extensive clinical trials normally in co-operation with a dental college or hospital departments prior to their release. CONCLUSION As the number of available materials is going up, it is important that the dentist remains more aware about new products so that their judgement about the selection of material remains successful. Materials which have not been thoroughly evaluated should be avoided, specially with clinical dentistry falling under Consumer Protection Act (CPA). I Research and development I iI Manufacturer/analysis Ideal requirements for clinical use: Thermal, optical, mechanical, chemical, biological Available materials and their properties are evaluated Launch of new I product Choice and selection of material by the dentist Critical assessment based on clinical performance I I H feedback to I
Crea un quiz con le seguenti domande. Inserisci anche la spiegazione. Domande Vero/Falso: 1. Vero o Falso: Se moltiplichiamo entrambi i membri di una disequazione per un numero negativo, il segno dell'ineguaglianza cambia. o Risposta: Vero o Spiegazione: Quando moltiplichiamo o dividiamo entrambi i membri di una disequazione per un numero negativo, il segno dell'ineguaglianza si inverte. 2. Vero o Falso: Una disequazione può avere solo una soluzione. o Risposta: Falso o Spiegazione: Una disequazione può avere zero, una o infinite soluzioni, a seconda dei valori coinvolti. 3. Vero o Falso: Se sommiamo o sottraiamo la stessa quantità da entrambi i membri di una disequazione, la soluzione rimane invariata. o Risposta: Vero o Spiegazione: Aggiungere o sottrarre la stessa quantità da entrambi i membri di una disequazione non cambia la relazione tra le soluzioni. 4. Vero o Falso: Se abbiamo una disequazione del tipo 2x>102x>10, la soluzione è x<5x<5. o Risposta: Vero o Spiegazione: Dividendo entrambi i membri per 22, otteniamo x>5/2x>5/2, che può essere semplificato a x>2.5x>2.5 o x>5/2x>5/2. 5. Vero o Falso: Una disequazione può avere solo numeri interi come soluzioni. o Risposta: Falso o Spiegazione: Le soluzioni di una disequazione possono essere numeri razionali o reali, non solo numeri interi. 6. Vero o Falso: Una disequazione del tipo 3x−2<53x−2<5 ha x>7/3x>7/3 come soluzione. o Risposta: Falso o Spiegazione: La soluzione corretta è x<7/3x<7/3 poiché 3x−23x−2 deve essere minore di 55, non maggiore. 7. Vero o Falso: Una disequazione del tipo 4x+7≥3x+54x+7≥3x+5 ha una soluzione unica. o Risposta: Vero o Spiegazione: Sottraendo 3x3x da entrambi i lati otteniamo x+7≥5x+7≥5, che semplificato diventa x≥−2x≥−2, quindi ha una soluzione unica. 8. Vero o Falso: Una disequazione quadratica è un tipo di disequazione di primo grado. o Risposta: Falso o Spiegazione: Una disequazione quadratica coinvolge il quadrato di una variabile e può essere di secondo grado o superiore, mentre una disequazione di primo grado coinvolge solo variabili elevate alla prima potenza. 9. Vero o Falso: Una disequazione del tipo 2(x−3)<82(x−3)<8 può essere risolta dividendo entrambi i membri per 22. o Risposta: Vero o Spiegazione: Dividendo entrambi i membri otteniamo x−3<4x−3<4, che può essere semplificato a x<7x<7 dopo l'aggiunta di 33 ad entrambi i membri. 10. Vero o Falso: Se abbiamo una disequazione del tipo x≤4x≤4 e x≥3x≥3, allora la soluzione è x=4x=4. o Risposta: Falso o Spiegazione: La soluzione è 3≤x≤43≤x≤4, il che significa che xx può essere qualsiasi numero tra 33 e 44, inclusi tutti i valori decimali in questo intervallo. Domande a Risposta Multipla: 11. Qual è la soluzione della disequazione 2x+5>112x+5>11? a) x<3x<3 b) x>3x>3 c) x<8x<8 d) x>8x>8 o Risposta: b) x>3x>3 o Spiegazione: Sottraendo 55 da entrambi i lati otteniamo 2x>62x>6, quindi x>3x>3. 12. Quale delle seguenti è una soluzione della disequazione 3x−1≤83x−1≤8? a) x=3x=3 b) x=1x=1 c) x=0x=0 d) x=4x=4 o Risposta: d) x=4x=4 o Spiegazione: Aggiungendo 11 ad entrambi i lati otteniamo 3x≤93x≤9, quindi x≤3x≤3. 13. Quale delle seguenti disequazioni è equivalente a 2(x+1)>62(x+1)>6? a) 2x>62x>6 b) 2x+2>62x+2>6 c) x+1>3x+1>3 d) x>2x>2 o Risposta: c) x+1>3x+1>3 o Spiegazione: Distribuendo 22 otteniamo 2x+2>62x+2>6, quindi x+1>3x+1>3. 14. Qual è la soluzione della disequazione 5x−4<3x+75x−4<3x+7? a) x<11x<11 b) x>11x>11 c) x<−11x<−11 d) x>−11x>−11 o Risposta: d) x>−11x>−11 o Spiegazione: Sottraendo 3x3x da entrambi i lati otteniamo 2x−4<72x−4<7, quindi 2x<112x<11 e infine x>−11x>−11. ……. 15 Qual è la soluzione della disequazione 2x+3≥5x−12x+3≥5x−1? a) x≤−1x≤−1 b) x≥−1x≥−1 c) x<2x<2 d) x>2x>2 o Risposta: c) x<2x<2 o Spiegazione: Sottraendo 5x5x da entrambi i lati otteniamo −3x+3≥−1−3x+3≥−1, quindi −3x≥−4−3x≥−4. Dividendo entrambi i lati per −3−3, ricordando di invertire il segno, otteniamo x<2x<2. 16 Quale delle seguenti è una soluzione della disequazione 4x−2≤2x+64x−2≤2x+6? a) x≤−2x≤−2 b) x≥−2x≥−2 c) x<2x<2 d) x>2x>2 o Risposta: b) x≥−2x≥−2 o Spiegazione: Sottraendo 2x2x da entrambi i lati otteniamo 2x−2≤62x−2≤6, quindi 2x≤82x≤8 e infine x≥−2x≥−2. 17 Quale delle seguenti è la soluzione della disequazione 3(x−2)>93(x−2)>9? a) x>3x>3 b) x>5x>5 c) x<3x<3 d) x<5x<5 o Risposta: b) x>5x>5 o Spiegazione: Dividendo entrambi i lati per 33, otteniamo x−2>3x−2>3, quindi x>5x>5. 18 Qual è la soluzione della disequazione 2x+4≤102x+4≤10? a) x≤2x≤2 b) x≥2x≥2 c) x<2x<2 d) x>2x>2 o Risposta: a) x≤2x≤2 o Spiegazione: Sottraendo 44 da entrambi i lati otteniamo 2x≤62x≤6, quindi x≤3x≤3. Tuttavia, dovremmo tenere conto che 22 è positivo, quindi la soluzione è x≤2x≤2. 19 Quale delle seguenti disequazioni è equivalente a 2x≤82x≤8? a) x≥4x≥4 b) x≤4x≤4 c) x>4x>4 d) x<4x<4 a. Risposta: b) x≤4x≤4 b. Spiegazione: Dividendo entrambi i lati per 22, otteniamo x≤4x≤4. 20 Quale delle seguenti è una soluzione della disequazione 5(x−3)>105(x−3)>10? a) x<−1x<−1 b) x>−1x>−1 c) x>5x>5 d) x<5x<5 a. Risposta: c) x>5x>5 b. Spiegazione: Dividendo entrambi i lati per 55, otteniamo x−3>2x−3>2, quindi x>5x>5.
Riferimenti normativi per il settore residenziale: Art 81: Accesso alla rete viaria—>> il cancello deve essere arretrato di almeno 4,5m dal filo esterno del marciapiede Art 82: Passo carrabile—>> larghezza non inferiore a 4,5m e non superiore a 6,5m Art 83:Pendenza Rampa —>> max 16% Art 97: Superficie minima degli ambienti - cucina —>> min 5mq - studio—>> min 7mq - soggiorno—>> min 14 mq - soggiorno spazi di cottura—>> 17 -camera (1posto letto)—>> 8mq - camera (2posti letto)—>> 12mq Superficie alloggio totale —>> non inferiore a 28 mq Art 95: Altezze minime- cucina, soggiorno, camera e studio—>> min 2,70m -locali accessori—>> min 2,40 m (bagno, lavanderie) - locali di servizio—>> min 2,10m (disimpegni, riposti.) - soppalchi—>> min 2,10m - parapetti—>> non inf. a 1,1m (10 cm cordolo) (92) Art 86: Distanze - negli edifici di nuova costruzione la distanza degli edifici dal confine con proprietà di terzi — nei NAF—>> non inf. a 3 m — altri ambiti —>> non inf. a 5m Art 89: Scale (R.E. ) —alzate—>> max 12 consecutive — a chiocciola—>> consentite solo all’interno di un’unità abit. — illuminazione—>> se collegano più di due piani devono . essere areati con lucernario. Dim: 0,3 mq . per ogni piano servito (R.I.: 0,4 mq x piano) — areazione —>> non ci può essere areazione verso i vani scala . ( Lo dice anche il regolamento d’igiene ) (R.I) —>> superficie non inferiore a 1mq per piano servi. — larghezza (R.I.) —>> deve garantire la possibilità di soccorso e . trasporto di persone Art 88: Locali sotterranei —>> non possono MAI essere adibiti ad abitazione Locali seminterrati—>> possono ma devono rispettare determinati . requisiti - l’altezza media deve essere > di 2,7m Art 91: Copertura—>> istallazione di apparati tecnici non deve essere visibile . dalle pubbliche vie Art 98: Bagni —>> ambiente contenente il vaso deve essere disimpegnato . dalla cucina (R.I: disimpegnato dai locali abitabili, esclusione Secondo bagno se è a servizio esclusivo di una camera) (R.I)—>> deve essere dotato di vaso, lavabo, bidet doccia o vasca —>> il lavabo può essere ubicato nell’antibagno Art 100: Areazione —>> riscontro d’aria deve essere garantito su aperture . perpendicolari o contrapposte.(non inf. a 1\10) —>> appartamenti inf. a 60mq possono essere . monoaffaccio ( ma non esposti a nord) Art 125: Raccolta rifiuti (R.E)—>> non meno di 0,18mq per ogni abitante . virtuale —>> non meno di 5 mq —>> altezza minima 2,4m (R.I: 2 m) —>> deve avere un punto di allacciamento d’acqua Regolamento d’igiene —>> dimensione tale da poter contenere 4,5l Di rifiuti per abitante.( in ogni caso > di 2mq) —>> scarichi sifonati dall’acqua di lavaggio —>> accorgimenti che assicurino un’adeguata Difesa antimurina e antinsetti Norma UNI 10750: superficie commerciale (ciò che compriamo) , cioè la somma delle superfici coperte—>> 100% delle superfici calpestatili —>>100% delle superfici su cui poggiano . Le pareti divisorie interne non portanti —>> 50% delle pareti portanti interne perimetrali —>> 25% delle aree non abitabili Superfici scoperte—>> 25% dei balconi e delle terrazze scoperte —>> 35% dei balconi e dei terrazzi coperti (3 lati) —>> 35% dei pati e dei porticati —>> 60% delle verande —>> 15% dei giardini di appartamento —>> 10% dei giardini di ville e villini (Se un muro è al confine con un altro appartamento lo considero dalla mezzeria, se confina con uno spazio comune idem, lo considero tutto invece se da sull’esterno ) Regolamento d’igiene (su esso prevale il Re) : norme che discipilinano degli aspetti della vita quotidiana al fine di tutelare la salute dei fruitori Si occupa di : Rumori , odori , fumi, vapori. Scarichi nel sottosuolo Pulizia e decoro Malattie infettive Igenicità degli ambienti Pareti trasparenti (tenendo conto di telai e infissi)—>> deve avere un area pari a 1\8 (nazionale), 1\10 (Milano ) della superficie di pavimento Profondità di pavimento—>> non deve superare i 2,5m dalla finestra Bagno cieco solo se la superficie lorda di pavimento è inferiore ai 70mq e se è presente una sola camera da letto , oppure se è un secondo bagno (altrimenti finestra > 0,5 apribile). Superficie illuminante—>> superficie totale dell’apertura meno - superficie finale non utile (C): 60 cm - superficie superiore non utile (A) A= va considerato per intero se non ci sono aggetti o se questi sono inferiori a 150 cm. Al contrario ne considero solo un terzo. Es: con aggetto, b+ 1\3a . Se il rapporto illuminante è rispettato la profondità del locale non può essere più di 2,5 volte l’altezza del voltino . Se non è rispettato (inferiore a 1\8) allora deve essere 3,5 volte Alloggi devono essere dotati— per 1\2 perone—>> 1 spazio cottura,1 servizio igienico , 1 ripostiglio — per 3\4 persone—>> 1 cucina indipendente, 1 servizio igienico , 1 ripostiglio — per 4\5 persone —>> 1 cucina indipendente, 2 servizi igienici, 1 ripostiglio (per il secondo servizio è richiesta una superficie minima di 2mq e un lato minimo di 1,2m) Dotazione dei servizi: Cucina—>> pavimenti e pareti con superficie Di materiale impermeabile, liscio, lavabile,resist. —>> soffitto materiale traspirante —>> cappa collegata a ogni punto di cottura (Vedi bagno su) Prevenzione incendi : definisce —dimensionamenti—accessi all’area (locali di intrattenimento e di pubblico Spettacolo —>> larghezza 3,5 —>> h libera 4m —>> raggio di svolta 13m —>> pendenza non sup al 10% —>> resist al carico almeno 20t —profondità locali —>> i locali al chiuso non possono Essere ubicati oltre il secondo piano Interrato (non oltre i 10m) . Questi se Sono tra i 7,5 e i 10 m devono essere Protetti da un’impianto sprinkler e Essere dotati di uscite sicure. — carichi d’incendio — comunicazione (locali di intrattenimento e di pubb. Spettacolo —>> locali possono comunicare con altre Attività purché dotate di filtri a prova di Fumo e di porte REI (ameno 30) (queste Non vanno cont nel comp. delle vie d’uscit) — compartimentazioni — autorimesse — comportamento al fuoco
Art 125: Raccolta rifiuti (R.E)—>> non meno di 0,18mq per ogni abitante . virtuale —>> non meno di 5 mq —>> altezza minima 2,4m (R.I: 2 m) —>> deve avere un punto di allacciamento d’acqua Regolamento d’igiene —>> dimensione tale da poter contenere 4,5l Di rifiuti per abitante.( in ogni caso > di 2mq) —>> scarichi sifonati dall’acqua di lavaggio —>> accorgimenti che assicurino un’adeguata Difesa antimurina e antinsetti Norma UNI 10750: superficie commerciale (ciò che compriamo) , cioè la somma delle superfici coperte—>> 100% delle superfici calpestatili —>>100% delle superfici su cui poggiano . Le pareti divisorie interne non portanti —>> 50% delle pareti portanti interne perimetrali —>> 25% delle aree non abitabili Superfici scoperte—>> 25% dei balconi e delle terrazze scoperte —>> 35% dei balconi e dei terrazzi coperti (3 lati) —>> 35% dei pati e dei porticati —>> 60% delle verande —>> 15% dei giardini di appartamento —>> 10% dei giardini di ville e villini (Se un muro è al confine con un altro appartamento lo considero dalla mezzeria, se confina con uno spazio comune idem, lo considero tutto invece se da sull’esterno ) Regolamento d’igiene (su esso prevale il Re) : norme che discipilinano degli aspetti della vita quotidiana al fine di tutelare la salute dei fruitori Si occupa di : Rumori , odori , fumi, vapori. Scarichi nel sottosuolo Pulizia e decoro Malattie infettive Igenicità degli ambienti Pareti trasparenti (tenendo conto di telai e infissi)—>> deve avere un area pari a 1\8 (nazionale), 1\10 (Milano ) della superficie di pavimento Profondità di pavimento—>> non deve superare i 2,5m dalla finestra Bagno cieco solo se la superficie lorda di pavimento è inferiore ai 70mq e se è presente una sola camera da letto , oppure se è un secondo bagno (altrimenti finestra > 0,5 apribile). Superficie illuminante—>> superficie totale dell’apertura meno - superficie finale non utile (C): 60 cm - superficie superiore non utile (A) A= va considerato per intero se non ci sono aggetti o se questi sono inferiori a 150 cm. Al contrario ne considero solo un terzo. Es: con aggetto, b+ 1\3a . Se il rapporto illuminante è rispettato la profondità del locale non può essere più di 2,5 volte l’altezza del voltino . Se non è rispettato (inferiore a 1\8) allora deve essere 3,5 volte
L'attentato alle Torri Gemelle dell'11 settembre 2001 è stato orchestrato dall'organizzazione terroristica al-Qaida, guidata da Osama bin Laden. Al-Qaida, un gruppo estremista islamico, aveva l'obiettivo di colpire gli Stati Uniti per una serie di motivi, tra cui la loro presenza militare in Medio Oriente, il sostegno a Israele e le politiche economiche e geopolitiche percepite come oppressive nei confronti dei Paesi musulmani. L'attacco ha coinvolto 19 terroristi, che hanno dirottato quattro aerei commerciali: due hanno colpito le Torri Gemelle a New York, un altro il Pentagono vicino a Washington, D.C., mentre il quarto, United Airlines Flight 93, è precipitato in un campo in Pennsylvania dopo che i passeggeri hanno tentato di riprendere il controllo dell'aereo. Osama bin Laden ha rivendicato la responsabilità dell'attentato, che ha provocato circa 3.000 morti e ha avuto un impatto duraturo sulla politica internazionale, portando alle guerre in Afghanistan e Iraq e a significativi cambiamenti nella sicurezza globale Il fatto che quattro aerei dirottati siano riusciti a deviare dalla loro rotta senza un immediato intervento da parte delle autorità aeree è legato a una serie di fattori: 1. **Dirottamenti inattesi**: Prima dell'11 settembre 2001, il protocollo per gestire i dirottamenti aerei era molto diverso. I dirottamenti aerei, quando accadevano, di solito erano gestiti attraverso negoziazioni e si presumeva che i dirottatori cercassero principalmente attenzione o denaro, non attacchi suicidi. Non c'era una preparazione specifica per l'eventualità che gli aerei venissero usati come armi. 2. **Interruzione delle comunicazioni**: I dirottatori hanno spento i transponder sugli aerei (dispositivi che inviano segnali radar con informazioni su altitudine e posizione), rendendo difficile per i controllori del traffico aereo tracciare con precisione gli aerei. Gli aerei risultavano ancora visibili sui radar primari, ma senza i dati specifici del transponder era difficile capire immediatamente che c'era una deviazione fuori rotta. 3. **Tempo di reazione**: Gli eventi si sono svolti in un breve arco di tempo. I primi segni di problemi sui voli sono emersi intorno alle 8:14 (con l'American Airlines Flight 11), e il primo schianto contro la Torre Nord è avvenuto alle 8:46. Tra l'inizio dei dirottamenti e gli impatti, il tempo per reagire è stato limitato. La portata dell'attacco era senza precedenti, e nessuno si aspettava che i dirottatori avrebbero usato gli aerei come armi contro obiettivi civili. 4. **Coordination failures**: Anche se ci sono stati segnali di problemi, la comunicazione tra le varie agenzie coinvolte (Federal Aviation Administration, NORAD, ecc.) non era ottimale. La procedura per attivare la difesa aerea in caso di dirottamento era complessa, e la possibilità che aerei civili venissero utilizzati come armi suicide non era contemplata nei protocolli. 5. **NORAD e tempi di risposta**: Il NORAD (North American Aerospace Defense Command), incaricato della difesa aerea, aveva una capacità limitata di intercettare rapidamente aerei dirottati nello spazio aereo interno. Prima dell'11 settembre, le operazioni di difesa erano concentrate su possibili minacce esterne, e non su attacchi interni. Anche quando i caccia furono inviati, era troppo tardi per impedire gli impatti. Questi fattori, combinati con l'incredulità che un tale attacco potesse realmente accadere, hanno reso possibile che quattro aerei fossero dirottati e usati come armi senza un intervento preventivo efficace. Dopo l'11 settembre, furono apportati significativi cambiamenti ai protocolli di sicurezza aerea per prevenire simili attacchi in futuro. L'idea che l'11 settembre abbia fornito un "pretesto" per attaccare l'Afghanistan è stata ipotizzata da diverse teorie del complotto e punti di vista critici sulla politica estera degli Stati Uniti. Tuttavia, è importante distinguere tra i fatti documentati e le ipotesi non verificate. ### Fatti documentati: 1. **Al-Qaida e Osama bin Laden**: Gli attacchi dell'11 settembre sono stati rivendicati da al-Qaida, che aveva il suo quartier generale in Afghanistan sotto la protezione del regime talebano. Gli Stati Uniti hanno chiesto ai talebani di consegnare Osama bin Laden, ma il governo talebano ha rifiutato. Questo ha portato all'intervento militare in Afghanistan con l'obiettivo dichiarato di smantellare al-Qaida e rimuovere i talebani dal potere. 2. **Legittimazione internazionale**: L'invasione dell'Afghanistan è stata ampiamente appoggiata a livello internazionale, con il sostegno delle Nazioni Unite e della NATO. Il Consiglio di Sicurezza delle Nazioni Unite ha approvato risoluzioni che condannavano gli attacchi e riconoscevano il diritto di difesa degli Stati Uniti. ### Teorie del complotto: Alcuni teorici sostengono che l'11 settembre potrebbe essere stato usato come pretesto per giustificare una guerra che rientrava in più ampi interessi geopolitici. Secondo questa visione, l'invasione dell'Afghanistan non riguardava solo la lotta contro il terrorismo, ma anche: - **Influenza geopolitica**: Gli Stati Uniti avrebbero cercato di stabilire una maggiore presenza militare e influenza in una regione strategica, vicina a Paesi come l'Iran, la Cina e la Russia. - **Risorse naturali**: L'Afghanistan ha un'importanza geopolitica anche per i suoi potenziali corridoi energetici e per le sue risorse minerarie, anche se non ha ricchezze petrolifere significative come altri Paesi del Medio Oriente. ### Critiche legittime: Al di là delle teorie del complotto, ci sono critiche legittime alla risposta degli Stati Uniti e all'espansione della guerra al terrorismo. Ad esempio: - **La guerra in Iraq**: Mentre l'invasione dell'Afghanistan fu largamente supportata, l'invasione dell'Iraq nel 2003 fu molto più controversa. Molti analisti ritengono che l'amministrazione Bush abbia sfruttato la paura generata dall'11 settembre per giustificare un attacco all'Iraq, anche se non c'erano prove concrete di un collegamento tra il regime di Saddam Hussein e al-Qaida. - **Durata della guerra**: La guerra in Afghanistan si è trasformata in un conflitto di lunga durata, che molti vedono come fallimentare, con risultati incerti nonostante il grande impegno militare ed economico. ### Conclusione: Sebbene sia possibile che alcune figure politiche o militari abbiano sfruttato l'attacco dell'11 settembre per portare avanti agende geopolitiche preesistenti, i fatti storici mostrano che l'invasione dell'Afghanistan fu una reazione diretta agli attacchi e alla minaccia di al-Qaida. Le decisioni successive, in particolare l'espansione della "guerra al terrorismo", sono state oggetto di forti critiche e controversie, ma non ci sono prove concrete che l'11 settembre sia stato pianificato o lasciato accadere per giustificare un'invasione. La **caduta delle Torri Gemelle** l'11 settembre 2001 è stata causata principalmente dai **danni strutturali provocati dall'impatto degli aerei e dal conseguente incendio**, secondo le indagini ufficiali. Le teorie che ipotizzano l'uso di esplosivi sono state ampiamente investigate ma smentite dalle analisi tecniche e dalle prove disponibili. ### Versione ufficiale: 1. **Impatto degli aerei**: Gli aerei di linea colpirono le Torri Gemelle a una velocità molto elevata, causando danni immediati e significativi alle colonne portanti esterne e interne degli edifici. Questi danni strutturali compromettevano già parte della stabilità delle torri. 2. **Incendi**: L'impatto degli aerei ha causato l'esplosione del carburante contenuto nei serbatoi, innescando vasti incendi. Il calore generato dagli incendi all'interno degli edifici raggiunse temperature estremamente elevate (fino a 1000°C o più), che indebolirono ulteriormente l'acciaio delle strutture portanti. 3. **Cedimento strutturale**: L'acciaio non deve necessariamente fondere per perdere la sua capacità portante; a temperature elevate, l'acciaio diventa più malleabile e perde resistenza. Questo, unito al danno meccanico già causato dall'impatto degli aerei, ha portato al cedimento progressivo delle strutture superiori, che sono collassate sui piani inferiori in una sorta di effetto domino. Questo spiega il "crollo verticale" delle torri. ### Investigazioni tecniche: 1. **Rapporto del NIST**: Il **National Institute of Standards and Technology (NIST)** ha condotto un'indagine approfondita sulla caduta delle torri. Secondo il rapporto del NIST, **non ci sono prove** che suggeriscano l'uso di esplosivi o ordigni nei crolli delle torri. I crolli sono stati attribuiti esclusivamente ai danni strutturali causati dagli impatti e agli incendi successivi. 2. **Simulazioni e analisi**: Gli ingegneri hanno simulato il comportamento degli edifici durante l'attacco e hanno concluso che l'indebolimento delle strutture portanti a causa del calore è stato sufficiente a spiegare il collasso. Il crollo avvenne in maniera progressiva e non con le caratteristiche di una demolizione controllata, come l'uso di esplosivi. ### Teorie del complotto: Nonostante le spiegazioni tecniche ufficiali, alcune persone sostengono che il crollo sia stato causato da esplosivi piazzati all'interno delle torri. Queste teorie si basano su: - **Testimonianze di esplosioni**: Alcune persone hanno riportato di aver sentito rumori di esplosioni prima o durante i crolli. Tuttavia, gli esperti hanno spiegato che questi rumori possono essere attribuiti a numerosi fattori, come i cedimenti strutturali e le esplosioni secondarie dovute al cedimento di infrastrutture interne (ad esempio, serbatoi di gas o trasformatori elettrici). - **Crollo simmetrico**: Alcuni teorici sostengono che il crollo delle torri sia stato troppo "ordinato" per essere casuale. Tuttavia, il collasso verticale è stato spiegato come il risultato del cedimento simultaneo di più colonne portanti indebolite dal calore. - **Teoria del crollo controllato**: Alcuni sostengono che le torri siano cadute con la rapidità e la precisione di una demolizione controllata. Tuttavia, studi dettagliati del NIST e altre organizzazioni non hanno trovato alcuna prova di esplosivi o segni di una demolizione pianificata. ### Conclusione: Le indagini ufficiali e i rapporti tecnici indicano chiaramente che il crollo delle Torri Gemelle è stato causato dagli impatti degli aerei e dai successivi incendi che hanno indebolito la struttura, portando al collasso progressivo. Le teorie che ipotizzano l'uso di esplosivi sono state esaminate ma non supportate da prove concrete. L'11 settembre 2001 ha avuto un impatto profondo anche sulla musica, influenzando artisti di diversi generi e portandoli a esprimere il dolore, la rabbia, la riflessione e la speranza che l'evento ha generato. La musica ha raccontato l'episodio da diverse prospettive, esplorando sia il trauma individuale che quello collettivo, e offrendo una forma di guarigione o commemorazione per chi l'ha vissuto. ### Canzoni che hanno affrontato l'11 settembre: 1. **Bruce Springsteen – "The Rising" (2002)** Questo album è uno dei più emblematici legati all'11 settembre. La title track, "The Rising", racconta la storia di un pompiere che sale verso le Torri Gemelle e riflette sul sacrificio e la speranza. L'intero album esplora i temi della perdita e della resilienza attraverso il prisma dell'America post-11 settembre, e rappresenta una sorta di catarsi per molte persone che hanno cercato conforto nella musica. 2. **Paul McCartney – "Freedom" (2001)** Paul McCartney era a New York il giorno degli attacchi e ha scritto questa canzone in risposta, cercando di trasmettere un messaggio di forza e resistenza. "Freedom" è stata eseguita al concerto benefico **"The Concert for New York City"**, un evento organizzato per raccogliere fondi per le vittime dell'attacco e celebrare il coraggio dei soccorritori. 3. **Toby Keith – "Courtesy of the Red, White and Blue (The Angry American)" (2002)** Questa canzone country ha rappresentato il lato più patriottico e arrabbiato della reazione americana agli attentati. Toby Keith esprime il desiderio di giustizia (o vendetta), e la canzone è diventata molto popolare tra coloro che volevano una risposta forte agli attacchi. Sebbene controversa per i suoi toni duri, ha rappresentato una parte significativa del sentimento nazionale. 4. **Alan Jackson – "Where Were You (When the World Stopped Turning)" (2001)** Questa ballata country ha cercato di catturare lo shock, la confusione e il dolore collettivo che l'11 settembre ha causato. La canzone pone domande che molti si sono fatti: "Dov'eri quando il mondo si è fermato?" Il tono è riflessivo e malinconico, ed è diventata una delle canzoni più ricordate che trattano direttamente dell'evento. 5. **U2 – "Walk On" (2001)** Sebbene scritta prima dell'11 settembre, "Walk On" è diventata una sorta di inno di resilienza dopo l'attacco. U2 ha dedicato diverse performance della canzone alle vittime dell'11 settembre, e il testo, che parla di andare avanti di fronte alle avversità, è stato interpretato come un messaggio di forza per chi cercava di ricostruire la propria vita. 6. **Neil Young – "Let’s Roll" (2001)** Questa canzone è stata ispirata dagli atti eroici dei passeggeri del volo United 93, che si sono ribellati contro i dirottatori, impedendo che l'aereo colpisse un obiettivo a terra. La frase "Let's roll" era ciò che uno dei passeggeri, Todd Beamer, ha detto mentre guidava la ribellione. Neil Young ha scritto questo brano per onorare quei passeggeri coraggiosi. ### Concerti e eventi musicali commemorativi: - **The Concert for New York City (2001)** Subito dopo gli attacchi, questo grande concerto benefico si è tenuto al Madison Square Garden per raccogliere fondi a favore delle vittime e per rendere omaggio ai soccorritori. Vi hanno partecipato artisti come Paul McCartney, The Who, Mick Jagger, David Bowie e molti altri. L'evento è stato una celebrazione dell'unità e della solidarietà di fronte alla tragedia. - **America: A Tribute to Heroes (2001)** Questo telethon, trasmesso a livello nazionale, ha visto la partecipazione di artisti come Bruce Springsteen, U2, Celine Dion e molti altri. Lo scopo era quello di raccogliere fondi per le vittime e i loro familiari, e molte delle performance erano riflessive e piene di emozione, offrendo un momento di unità e commiserazione collettiva. ### Effetti sull’industria musicale: L'11 settembre ha avuto anche un impatto diretto sull'industria musicale: - **Censura e sensibilità**: Molte canzoni che potevano essere considerate inappropriate o troppo aggressive dopo l'11 settembre furono temporaneamente rimosse dalle playlist radiofoniche, come "Imagine" di John Lennon (per il suo messaggio pacifista) o "New York, New York" di Frank Sinatra, per il legame con la città colpita. - **Modifiche ai testi e alle copertine**: Alcuni artisti modificarono testi o copertine di album che potevano sembrare insensibili o inappropriate nel clima post-11 settembre. Ad esempio, i Dream Theater cambiarono la copertina del loro album "Live Scenes from New York" perché raffigurava il World Trade Center in fiamme, una coincidenza che uscì pochi giorni prima degli attacchi. ### Conclusione: La musica ha offerto un modo per elaborare il trauma dell'11 settembre, sia attraverso canzoni che commemorano i caduti, sia con inni che hanno ispirato resistenza e speranza. Artisti di ogni genere hanno interpretato l'evento in modi diversi, riflettendo la complessità delle emozioni che ha suscitato, dall'angoscia e la perdita alla forza e la solidarietà. Sì, le **Dixie Chicks** (oggi conosciute come **The Chicks**) hanno avuto notevoli problemi, ma non per aver trattato direttamente il tema dell'11 settembre. I problemi che hanno affrontato sono legati alle loro critiche alla guerra in Iraq e alla presidenza di **George W. Bush**, che erano strettamente connesse al clima politico post-11 settembre. ### Contesto: Nel marzo 2003, durante un concerto a Londra, la cantante **Natalie Maines**, frontwoman delle Dixie Chicks, fece una dichiarazione che scatenò una controversia a livello nazionale negli Stati Uniti. Mentre l'invasione dell'Iraq era imminente, Maines disse al pubblico: > **"Just so you know, we’re ashamed that the President of the United States is from Texas."** Questa dichiarazione era una critica diretta al presidente **George W. Bush**, nato in Texas come Maines e il resto della band. La critica arrivava in un momento in cui il patriottismo e il sostegno alla guerra erano fortemente presenti negli Stati Uniti, specialmente nel Sud, dove le Dixie Chicks avevano una vasta base di fan nella comunità country. ### Conseguenze: 1. **Boicottaggi e censure**: Dopo il commento di Maines, molte stazioni radio, soprattutto quelle country, **boicottarono le Dixie Chicks**, rimuovendo le loro canzoni dalle playlist. In alcune parti degli Stati Uniti, i fan organizzarono pubblici **roghi dei loro album**. 2. **Perdita di supporto nel mondo country**: La comunità della musica country, che spesso riflette valori patriottici e conservatori, si rivolse contro di loro. Molti artisti e fan country criticarono duramente le Dixie Chicks per aver espresso opinioni contro la guerra e contro il presidente in un momento in cui il sostegno alla leadership nazionale era considerato importante. 3. **Minacce e ostilità**: Le Dixie Chicks ricevettero **minacce di morte** e furono soggette a intense campagne di odio. Questo dimostrò quanto fossero polarizzate le opinioni politiche negli Stati Uniti all'epoca, specialmente nell'industria della musica country. 4. **Carriera messa in pausa**: Dopo la controversia, la loro carriera negli Stati Uniti subì un grave colpo. Le vendite dei loro album calarono, e per diversi anni furono considerate una "band alienata" dall'industria country. Tuttavia, il gruppo trovò maggiore supporto nel pubblico internazionale e in generi musicali non tradizionalmente legati al country. ### La risposta delle Dixie Chicks: Le Dixie Chicks risposero alla controversia con coraggio e determinazione. Nel 2006, pubblicarono l'album **"Taking the Long Way"**, che includeva la famosa canzone **"Not Ready to Make Nice"**. Questo brano affrontava direttamente le critiche ricevute e il loro rifiuto di scusarsi per aver espresso le proprie opinioni. > **"Not Ready to Make Nice"** fu un grande successo e vinse diversi Grammy Awards, incluso quello per il **Miglior Album dell'Anno** e la **Canzone dell'Anno**. L'album rappresentava un chiaro messaggio: non erano pronte a cedere alla pressione e non si scusavano per aver esercitato la loro libertà di espressione. ### Riflessione sulla controversia: La controversia rifletteva una tensione più ampia nella società americana post-11 settembre, dove il patriottismo era visto da molti come un valore sacro e la critica alle politiche governative, specialmente riguardo alla guerra, poteva essere percepita come un tradimento. Le Dixie Chicks divennero un simbolo di questa polarizzazione e del conflitto tra libertà di espressione e patriottismo. ### Conclusione: Sebbene le Dixie Chicks non abbiano trattato direttamente l'11 settembre, la loro critica alla guerra in Iraq e a George W. Bush, strettamente connessa agli eventi post-11 settembre, portò a una delle più grandi controversie nella storia della musica country. Tuttavia, con il tempo, il gruppo è riuscito a superare le difficoltà e ha ottenuto una sorta di redenzione artistica e pubblica, guadagnando il rispetto di molti per la loro integrità e il loro coraggio nel difendere le proprie opinioni. Sì, i **Green Day** hanno trattato indirettamente i temi legati all'11 settembre e le sue conseguenze, soprattutto attraverso il loro album più famoso, **"American Idiot"** (2004). L'album non affronta direttamente gli attacchi dell'11 settembre, ma esplora il clima politico e sociale che si è sviluppato negli Stati Uniti dopo gli attentati, in particolare la guerra in Iraq, il patriottismo estremo e la manipolazione dei media. ### Contesto di "American Idiot": "American Idiot" è un concept album che segue un personaggio chiamato **Jesus of Suburbia**, che rappresenta la frustrazione e l'alienazione della generazione cresciuta nell'America post-11 settembre. L'album racconta una storia di rabbia, disillusione e ribellione contro il governo, i media e la società americana dell'epoca. ### Temi principali legati all'11 settembre e alle sue conseguenze: 1. **Critica ai media e alla manipolazione dell'informazione**: - La title track, **"American Idiot"**, critica aspramente la manipolazione dei media e il modo in cui la società americana è stata spinta verso un patriottismo cieco e un clima di paura. La canzone si scaglia contro l'idea che gli americani vengano indotti a seguire passivamente le direttive dei media e del governo, un tema strettamente legato alla narrazione post-11 settembre e alla propaganda che ha accompagnato la guerra in Iraq. > "Don't wanna be an American idiot, Don't want a nation under the new media." Qui, la band esprime il loro disgusto per l'influenza della propaganda mediatica e la crescente polarizzazione politica. 2. **Disillusione verso il governo e la guerra**: - Il brano **"Holiday"** è una feroce critica alla guerra in Iraq e alla politica estera dell'amministrazione Bush, spesso vista come una conseguenza diretta degli attacchi dell'11 settembre. La canzone denuncia l'ipocrisia e l'avidità che, secondo i Green Day, hanno guidato la decisione di invadere l'Iraq. > "This is the dawning of the rest of our lives, On holiday." Il termine "holiday" viene usato sarcasticamente per indicare una pausa dalla realtà, mentre la guerra viene condotta senza una giustificazione morale valida. 3. **Riflessioni sulla paura e l'ansia della generazione post-11 settembre**: - **"Boulevard of Broken Dreams"** esplora temi più personali di alienazione e solitudine, ma riflette anche l'ansia e la disillusione che molti americani, specialmente giovani, hanno provato nell'era post-11 settembre. Il senso di isolamento e la perdita di speranza di Jesus of Suburbia rappresentano simbolicamente il malessere di una generazione confusa e incerta sul futuro. > "I walk a lonely road, The only one that I have ever known." 4. **Rabbia verso l'apatia sociale**: - In **"Wake Me Up When September Ends"**, molti hanno visto una connessione simbolica con gli attacchi dell'11 settembre. Sebbene la canzone sia stata scritta dal frontman **Billie Joe Armstrong** come una riflessione personale sulla morte di suo padre, è diventata una sorta di inno per chiunque cercasse di elaborare il dolore e il trauma degli eventi del 2001. L'uso di "September" nel titolo ha portato molti a collegare il brano agli eventi dell'11 settembre e al desiderio di superare quel periodo buio. > "Here comes the rain again, Falling from the stars, Drenched in my pain again, Becoming who we are." La canzone evoca sentimenti di perdita e desiderio di guarigione, temi che risuonano con l'atmosfera post-attentati. ### Impatto di "American Idiot": "American Idiot" è stato un successo enorme e ha avuto un impatto culturale significativo. L'album ha dato voce a una generazione di giovani disillusi dalla politica americana e dalla guerra, riflettendo il malcontento diffuso verso l'amministrazione Bush e il modo in cui il paese aveva reagito agli eventi dell'11 settembre. Il successo dell'album ha portato anche alla produzione di un musical omonimo, che ha continuato a esplorare questi temi. ### Conclusione: I Green Day non hanno trattato direttamente gli attacchi dell'11 settembre, ma il loro album "American Idiot" è una risposta critica alle conseguenze politiche e sociali di quell'evento, in particolare la guerra in Iraq, la manipolazione dei media e la disillusione dei giovani. L'album è stato un potente veicolo di protesta contro il clima politico dell'epoca e ha dato voce alla frustrazione di molti americani.