Loading...

1.6 Metabolic pathways
Quiz by Richie Lambert
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
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 DesirĂŠe Nieuwenhuis | NatĂ lia 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. Š 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-Îą 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- Îą 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-Îą 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-Îą, 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-Îą 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-Îą, 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)â 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 âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, 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, WidĂŠn 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) 1999â2004. 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, SchĂśnbeck 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. BĂśttner A, Jr K, MĂźller 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, IĂąiguez 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 âobesity paradoxâ 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
Acetic acid â a chemical substance with an inhibiting effect on the growth of microorganisms and which is present in vinegar.Acetic Acid Fermentation Fermentation preserves food through the metabolic activities of selected groups of microorganisms. During the process, compounds such as lactic acid, acetic acid and alcohol are developed and result in a more or less stable food form. It makes food more nutritious as dietary source of proteins, vitamins and minerals.Vinegar is an example of the product of acetic acid fermentation which also undergoes alcoholic fermentation to complete the process.Filter â is a device, substance (like paper or charcoal), or process that separates unwanted components from a fluid Cheesecloth-is a loose-woven, gauze-like cotton fabric used for straining liquids from solids.Decant- gradually pour (liquid, typically wine or a solution) from one container into another, especially without disturbing the sediment. Sediment-is solid material (like sand, silt, clay, rocks, organic matter) broken down by weathering, transported by wind, water, or ice, and deposited in a new location, settling at the bottom of water bodies or on land.How to make vinegar?1.Grind or crash the fruit, then boil in water of the same amount as the ground flesh, peels and cores. Boil until soft, and then strain the juice through a cheesecloth2.Add Âź (one-fourth) pound of sugar for every liter of juice extracted from fruit peels and cores. Do not add sugar when using ripe fruit.3.Add Âź of a cake of fresh yeast that has been well-broken up, for every liter of juice. Stir very well, and then place in glass jars. Cover with a clean cloth and let the mixture stand for about two weeks .4. After two weeks, separate the clear liquid from the sediment. Prepare fresh, unpasteurized vinegar also called âmother vinegarâ which is the white gummy mass that usually forms in vinegar. Add this to the liquid and mix very well. Over the container with cloth, then allow to stand in a warm place until it has acquired a flavor strong enough to use.5.Filter the clear liquids, then pour in a bottle and cover tightly.USES OF VINEGAR1. Insect salve and repellent. 2. Kill weeds and remove ants. 3. Enhance bricks. 4.Open a tight jar. 5.Clean scissors. 6.Remove smoke odors. 7. Remove pit stains. 8. Make hair shine. 9. Fruit fly trap. 10. Car care.Â
[t comes from the GREEK name "Epilepsia" which means "taking hold of or seizing". - It is a disorder characterized by: recurrent seizures. SEIZURES R ectment transient attacks of: R epresent: R esult from: ASSOCIATED WITH: somatic, psychic, or, autonomic clinical featmes. clinical features of abnormally hyperexcitable cortical neurons. paroxvsmal and excessive electrical neuronal discharges. EEG changes & may be disturbance of consciousness. same causes of convulsions 1. Idiopathic epile~ ⢠It is the commonest cause. no cause can be detected ( 65 % ) ⢠It may be associated with positive family history in some cases. ⢠It starts in the l st & 2nd decades in the form of: -- Grand ma! epilepsy. Petit mal epilepsy. Myoclonic epilepsy. Atonic seizures. 2. Secondary epilepsy A. Local causes in the brain: l. Congenital: 2. Traumatic: cerebral palsy. a cause can be detected cerebral contusion or laceration. 3. Inflammatory: 4. Neoplastic: 5. Degenerative: 6. Vascular: encephalitis, brain tumours. mening1t1s, presenile dementia. brain abscess. stroke (especially hemon-hagic), hypertensive encephalopathy. B. General causes with secondary effects on the brain: I. Toxic: 2. Iatrogenic: 3. Metabolic: 4. Endocrinal: 5. Organ failure: 6. Heart disease: 7. Nutritional: - Alcohol, cocaine, lead. - Lidocaine, INH. - j glucose & ! glucose. - Hypoparathyroidism. - Hepatic failme. - Adam's Stoke's attacks. - Pellagra. - Botulism, tetanus. - Ambilhar, Amphetamine, Aminophylline. - j Ca & ! Ca. - Hype1thyroid crisis. - Renal failure. - Fallot's tetralogy. - j Na & ! Na. - Vitamin B6 deficiency. 8. Physical: 9. HYSTERICAL. - High fevers. - Heat stroke. 136 137 CLINICAL PICTURE 1. GENERALISED SEIZURES " Excessive electrical discharges from cortical neurons in BOTH hemispheres simultaneously " I. II. 1. Grand Mal Epile~: 1. Pre-ictal stage "attacks of tonic-clonic convulsions " (aura) It is a warning sign of a coming attack. It may be: ⢠Somatic: ⢠Psychic: ⢠Autonomic: 2. Ictal stage Myoclonus, Hallucinations. Tachycardia, (seizure) Sudden loss of consciousness: Parasthesias. Sweating. for seconds to minutes. -- Tonic phase (few seconds) o The UL & LL: o o o o The HEAD: The JAWS: CYANOSIS: are extended. is retracted to one side & the eye balls rolled up. are firmly clenched, with biting of the TONGUE. due to impaired respiration. There may be incontinence of urine. Clonic phase (few minutes) o The UL & LL: o The HEAD: 3. Post-ictal stage - It may be: ⢠Somatic: ⢠Psychic: ⢠Autonomic: Drug of choice: contract & relax repeatedly & rapidly. jerks forcibly. (sequelae) Todd's paralysis(< 24 hours, due to neuronal exhaustion). Confusion. Vomiting. Carbamazepine (Tegretol) or Phenytoin (Epanutin) Petit Mal Epilepsy: "attacks of loss of consciousness " " Absence " It starts in childhood & improves at puberty & usually disappears at the age of 20. 2. It is NOT PRECEEDED by aura & NOT FOLLOWED by sequelae. 3. It is usually PRECIPITATED by: hyperventilation 4. It is characterized by: or photic stimulation. sudden loss of consciousness of short duration (few seconds). 5. It may be associated with: ⢠High frequency ( 50 attacks / day). ⢠Falling to the ground without warning. ⢠Jerky movements of the head & UL Drug of choice: (myoclonic petit mal). Valproate (Depakine) or Succinimide (Zarontin) 137 138 Ill. M oclonic Seizures: "attacks of involuntary clonic movements " - It is characterized by: sudden, jerky, shock-like INVOLUNTARY muscle contraction. ⢠The jerks are bilateral contractions, mainly of the shoulders and arms. ⢠However, some patients repmtjerking in the lower limbs, trunk, or head. - It may be of 2 types: - Occurs singly ⢠Simple: ⢠As a pait of: I Drug of choice: IV. Atonic seizures: (no loss of consciousness). - Grand mal epilepsy (aura). - Petit mal epilepsy. Valproate (Depakine) or Clonazepam (Rivotril) I - Transient attacks of brief loss of postural tone, often resulting in falls and injuries. 2. PARTIAL SEIZURES "Excessive electrical discharges from cmtical neurons in a ce1tain area in ONE hemisphere" A. Simple seizures: " No disturbance in consciousness " - The CP depends on the site of the hyperexcitable neurones in the cerebral cortex, whether in: "Motor area or Senso,y areas". 1. Motor fits: ⢠Focal fits: ⢠Motor jacksonian fits: 2. General Sensory fits: ⢠Focal fits: ⢠Sensory jacksonian fits: 3. Special Senso1y fits: ⢠Visual hallucinations: ⢠Auditory hallucinations: ⢠Olfactory hallucinations: B. Complex seizures: - SITE: movement of part of a limb or the whole limb. movement of one side of the body (see before). parasthesia of part of a limb or the whole limb. parasthesia of one side of the body (see before). irritation of the visual sensory area. irritation of the auditory sensory area. initation of the uncus. " disturbance in consciousness " The hyperexcitable neurons are in the Temporal lobe "Temporal lobe epilepsy". - DURATION: The seizure lasts few seconds to few minutes. - The seizure starts with A ura, followed by A bsence, Automatism, Amnesia: 1. 2. 3. 4. A ura: A bsence: Automatism: A mnesia: Olfactory hallucinations, Deja-vu phenomenon, Sensation of fear. Absent patient with staring eyes (with no response to conversation). Involuntary Purposeless acts: motor ( eg, lip smacking, chewing) or verbal. No recalling of the seizure. 138 139 3. PARTIAL SEIZURES ~ GENERALISED SEIZURES " Partial seizures may spread to involve the whole brain .- secondarily generalised seizures " . HY-sterical epilepsY ⢠Usually: ⢠The cause: ⢠Incidence: young neurotic Sj2 . psychological & there is no organic lesion. usually occurs in the presence of people. ⢠It is associated with: ⢠EEG: ⢠It is not associated with: normal. ⢠Missed ttt. ⢠Menses. ⢠Alkalosis. anxiety, palpitaion & hyperventilation. tongue biting or incontinence of urine. ⢠Alcohol use & Drug abuse ( e.g. cocaine ). ⢠S timulation by photons & Hyperventilation. ⢠S leep deprivation & Stress & sudden withdrawal of antiepileptic drngs. INVESTIGATIONS 1. EEG: ⢠It is the most specific test for epilepsy because it records the electrical activity of the brain. ⢠It shows specific pattern: 2. LOCAL INVESTIGATIONS: "Epilepsy waves". "CT & MRI of the brain" ⢠To identify or exclude a LOCAL CAUSE of seizures in the brain. 3. GENERAL INVESTIGATIONS: "Laboratory investigations" ⢠To search for a GENERAL CAUSE of seizures, e.g. blood glucose. 139 140 TREATMENT A. General Measures: 1. 2. Moderation of the patient's physical activity. A void the precipitating factors ( Alcohol, hyperventilation, photic stimulation ...... ). 3. A ketogenic diet is encouraged because it will induce acidosis: - Acidosis is beneficial as it raises the threshold of stimulation of the brain cells. B. Specific Treatment: 2. 1. Treatment of the cause in secondary epilepsy. Anti-epileptic drugs: a) Always sta1t with one drug, then add another drug if there is no response. b) Always stop the drugs ONLY if: ⢠The patient stays free of symptoms for at least 2 years. ⢠The patient has a normal EEG. 3. Side effects of Anti-epileptic drugs: I . Skin rash. 2. 3. Bone marrow depression. Ataxia. Drug 1. Barbiturates (Pbenonobarbitone) 2. Hydantoin (Epanutin) 3. Carbamazepine 4. Clonazepam 5. Valproate 6. Succinamide ANTI-EPILEPTIC DRUGS NEW ANTI-EPILEPTIC DRUGS - These drugs are new dtugs that may be used in resistant seizures. 1. Lamotrigine: 200 - 400 mg/ day. 2. Felbamate: 3. Gabapentin: 400- 800 mg/ day. 600 - 1200 mg/ day. \ " General rules for use ": Dose 100-600 mg I day 100-600 mg / day 200-600 mg I day 2-6 mg I day 500-1500 mg I day 500-1000 mg / day Best indicated - Broad spectrum. - Not for petit mal. - Grand mal. - Motor Jacksonian fits. - Grand mal. - Motor Jacksonian fits. - Complex seizures. - Not for petit ma!. - Myoclonic. - Grand mat. - Broad spectrum. - Petit mat. 140 141 STATUS EPILEPTICUS DEFINITION - A medical emergency: 1. Repeated attacks of generalized convulsions, with lack of recove,y of consciousness, 2. Persistent attack of seizure lasting for at least 30 minutes. OR, - If the convulsions are not stopped rapidly, coma deepens & death may occur due to: heart failure or respiratory failure or brain damage or hyperpyrexia. - The most common causes are: sudden withdrawal of anti-epileptic drugs & stroke. TREATMENT A. General Measures: l. Take care of: " ABC " ⢠Place the patient on the ground, to guard against falling from bed. ⢠Mouth gag & 02 inhalation ( endo-tracheal intubation may be needed). ⢠Record the vital signs regularly. 2. Take a sample of: - Venous blood: for the level of: - A.tierial blood: for the level of: 3. a nti-epileptic drugs, a lcohol. pH, p0 2, pC02, HC0 3. Give cerebral dehydrating measures: e.g. Frusemide, cone. Mannitol, Dexamethazone. B. Specific Treatment: - Phenytoin with diazepam (or clonazepam) immediately: 1. Phenytoin: 2. Diazepam: Clonazepam: seizures recur: 15 mg I Kg slow infusion. 5 mg slowly IV, to be repeated after 5 minutes if seizures recur: maximum dose: 20 mg. OR: 2 mg slowly IV, to be repeated after 5 minutes if maximum dose: 6 mg. - If seizures persist after 20 min. of Phenytoin & diazepam: 3. PHENOBARBITONE: - In resistant cases: 200 mg infusion. 4. GENERAL ANAESTHESIA: may be used.
In many cases, cells must move materials from an area of lower concentration to an area of higher concentration, or âupâ their concentration gradient. Such movement of materials is known as active transport. Unlike passive transport, active transport requires a cell to expend energy. CELL MEMBRANE PUMPS Ion channels and carrier proteins not only assist in passive trans- port but also help with some types of active transport. The car- rier proteins that serve in active transport are often called cell membrane âpumpsâ because they move substances from lower to higher concentrations. Carrier proteins involved in facilitated diffusion and those involved in active transport are very similar. In both, the molecule first binds to a specific kind of carrier protein on one side of the cell membrane. Once it is bound to the molecule, the protein changes shape, shielding the molecule from the hydrophobic interior of the phospholipid bilayer. The protein then transports the molecule through the membrane and releases it on the other side. However, cell membrane pumps require energy. Most often the energy needed for active transport is supplied directly or indirectly by ATP. Sodium-Potassium Pump One example of active transport in animal cells involves a carrier protein known as the sodium-potassium pump. As its name sug- gests, this protein transports Na ions and K ions up their con- centration gradients. To function normally, some animal cells must have a higher concentration of Na ions outside the cell and a higher concentration of K ions inside the cell. The sodium- potassium pump maintains these concentration differences. Follow the steps in Figure 5-6 on the next page to see how the sodium-potassium pump operates. First, three Na ions bind to the carrier protein on the cytosol side of the membrane, as shown in step . At the same time, the carrier protein removes a phosphate group from a molecule of ATP. As you can see in step , the phos- phate group from the ATP molecule binds to the carrier protein. Step shows how the removal of the phosphate group from ATP supplies the energy needed to change the shape of the carrier pro- tein. With its new shape, the protein carries the three Na ions through the membrane and then forces the Na ions outside the cell where the Na concentration must remain high. 3 2 1 SECTION 2 OBJECTIVES â Distinguish between passive transport and active transport. â Explain how the sodium-potassium pump operates. â Compare endocytosis and exocytosis. VOCABULARY active transport sodium-potassium pump endocytosis vesicle pinocytosis phagocytosis phagocyte exocytosis www.scilinks.org Topic: Active Transport Keyword: HM60018 mb06se_homs02.qxd 5/18/07 11:02 AM Page 103 104 CHAPTER 5 K+ K+ K+ K+ K+ K+ INSIDE OF CELL OUTSIDE OF CELL Carrier protein Cell membrane P P P P Na+ Na+ Na+ ATP ADP Na+ Na+ Na+ Na+ Na+ Na+ 1 2 3 4 5 6 At this point, the carrier protein has the shape it needs to bind two K ions outside the cell, as step shows. When the K ions bind, the phosphate group is released, as indicated in step , and the carrier protein restores its original shape. As shown in step this time, the change in shape causes the carrier protein to release the two K ions inside the cell. At this point the carrier protein is ready to begin the process again. Thus, a complete cycle of the sodium-potassium pump transports three Na ions out of the cell and two K ions into the cell. At top speed, the sodium-potassium pump can transport about 450 Na ions and 300 K ions per second. The exchange of three Na ions for two K ions creates an electrical gradient across the cell membrane. That is, the outside of the membrane becomes positively charged relative to the inside of the membrane, which becomes relatively negative. In this way, the two sides of the cell membrane are like the positive and nega- tive terminals of a battery. This difference in charge is important for the conduction of electrical impulses along nerve cells. The sodium-potassium pump is only one example of a cell membrane pump. Other pumps work in similar ways to transport important metabolic materials across cell membranes.
What is a Plant Cell? Plant cells are eukaryotic cells that vary in several fundamental factors from other eukaryotic organisms. Both plant and animal cells contain a nucleus along with similar organelles. One of the distinctive aspects of a plant cell is the presence of a cell wall outside the cell membrane. Plant Cell Structure Just like different organs within the body, plant cell structure includes various components known as cell organelles that perform different functions to sustain itself. These organelles include: Cell Wall It is a rigid layer which is composed of polysaccharides cellulose, pectin and hemicellulose. It is located outside the cell membrane. It also comprises glycoproteins and polymers such as lignin, cutin, or suberin. The primary function of the cell wall is to protect and provide structural support to the cell. The plant cell wall is also involved in protecting the cell against mechanical stress and providing form and structure to the cell. It also filters the molecules passing in and out of it. The formation of the cell wall is guided by microtubules. It consists of three layers, namely, primary, secondary and the middle lamella. The primary cell wall is formed by cellulose laid down by enzymes. Cell membrane It is the semi-permeable membrane that is present within the cell wall. It is composed of a thin layer of protein and fat. The cell membrane plays an important role in regulating the entry and exit of specific substances within the cell. For instance, cell membrane keeps toxins from entering inside, while nutrients and essential minerals are transported across. Nucleus The nucleus is a membrane-bound structure that is present only in eukaryotic cells. The vital function of a nucleus is to store DNA or hereditary information required for cell division, metabolism and growth. 1. Nucleolus: It manufactures cellsâ protein-producing structures and ribosomes. 2. Nucleopore: Nuclear membrane is perforated with holes called nucleopore that allow proteins and nucleic acids to pass through. Plastids They are membrane-bound organelles that have their own DNA. They are necessary to store starch and to carry out the process of photosynthesis. It is also used in the synthesis of many molecules, which form the building blocks of the cell. Some of the vital types of plastids and their functions are stated below: Leucoplasts They are found in the non-photosynthetic tissue of plants. They are used for the storage of protein, lipid and starch. Chromoplasts They are heterogeneous, colored plastid which is responsible for pigment synthesis and for storage in photosynthetic eukaryotic organisms. Chromoplasts have red-, orange- and yellow-colored pigments which provide color to all ripe fruits and flowers. Central Vacuole It occupies around 30% of the cellâs volume in a mature plant cell. Tonoplast is a membrane that surrounds the central vacuole. The vital function of the central vacuole apart from storage is to sustain turgor pressure against the cell wall. The central vacuole consists of cell sap. It is a mixture of salts, enzymes and other substances. Golgi Apparatus They are found in all eukaryotic cells, which are involved in distributing synthesized macromolecules to various parts of the cell. Ribosomes They are the smallest membrane-bound organelles which comprise RNA and protein. They are the sites for protein synthesis, hence, also referred to as the protein factories of the cell. Mitochondria They are the double-membraned organelles found in the cytoplasm of all eukaryotic cells. They provide energy by breaking down carbohydrate and sugar molecules, hence they are also referred to as the âPowerhouse of the cell.â Lysosome Lysosomes are called suicidal bags as they hold digestive enzymes in an enclosed membrane. They perform the function of cellular waste disposal by digesting worn-out organelles, food particles and foreign bodies in the cell. In plants, the role of lysosomes is undertaken by the vacuoles. Chloroplasts It is an elongated organelle enclosed by phospholipid membrane. The chloroplast is shaped like a disc and the stroma is the fluid within the chloroplast that comprises a circular DNA. Each chloroplast contains a green colored pigment called chlorophyll required for the process of photosynthesis. The chlorophyll absorbs light energy from the sun and uses it to transform carbon dioxide and water into glucose. Structure of Chloroplast Chloroplasts are found in all higher plants. It is oval or biconvex, found within the mesophyll of the plant cell. The size of the chloroplast usually varies between 4-6 Âľm in diameter and 1-3 Âľm in thickness. They are double-membrane organelle with the presence of outer, inner and intermembrane space. There are two distinct regions present inside a chloroplast known as the grana and stroma. ⢠Grana are made up of stacks of disc-shaped structures known as thylakoids or lamellae. The granum of the chloroplast consists of chlorophyll pigments and are the functional units of chloroplasts. ⢠Stroma is the homogenous matrix which contains grana and is similar to the cytoplasm in cells in which all the organelles are embedded. Stroma also contains various enzymes, DNA, ribosomes, and other substances. Stroma lamellae function by connecting the stacks of thylakoid sacs or grana. The chloroplast structure consists of the following parts: Membrane Envelope It comprises inner and outer lipid bilayer membranes. The inner membrane separates the stroma from the intermembrane space. Intermembrane Space The space between inner and outer membranes. Thylakoid System (Lamellae) The system is suspended in the stroma. It is a collection of membranous sacs called thylakoids or lamellae. The green colored pigments called chlorophyll are found in the thylakoid membranes. It is the sight for the process of light-dependent reactions of the photosynthesis process. The thylakoids are arranged in stacks known as grana and each granum contains around 10-20 thylakoids. Stroma It is a colorless, alkaline, aqueous, protein-rich fluid present within the inner membrane of the chloroplast present surrounding the grana. Grana Stack of lamellae in plastids is known as grana. These are the sites of conversion of light energy into chemical energy. Chlorophyll It is a green photosynthetic pigment that helps in the process of photosynthesis. Functions of Chloroplast Following are the important chloroplast functions: ⢠The most important function of the chloroplast is to synthesize food by the process of photosynthesis. ⢠Absorbs light energy and converts it into chemical energy. ⢠Chloroplast has a structure called chlorophyll which functions by trapping the solar energy and is used for the synthesis of food in all green plants. ⢠Produces NADPH and molecular oxygen (O 2 ) by photolysis of water. ⢠Produces ATP â Adenosine triphosphate by the process of photosynthesis. ⢠The carbon dioxide (CO2) obtained from the air is used to generate carbon and sugar during the Calvin Cycle or dark reaction of photosynthesis. Mitochondria âMitochondria are membrane-bound organelles present in the cytoplasm of all eukaryotic cells, that produce adenosine triphosphate (ATP), the main energy molecule used by the cell.â What are Mitochondria? Popularly known as the âPowerhouse of the cell,â mitochondria (singular: mitochondrion) are a double membrane-bound organelle found in most eukaryotic organisms. They are found inside the cytoplasm and essentially function as the cellâs âdigestive system.â They play a major role in breaking down nutrients and generating energy-rich molecules for the cell. Many of the biochemical reactions involved in cellular respiration take place within the mitochondria. The term âmitochondrionâ is derived from the Greek words âmitosâ and âchondrionâ which means âthreadâ and âgranules-likeâ, respectively. It was first described by a German pathologist named Richard Altmann in the year 1890. Structure of Mitochondria ⢠The mitochondrion is a double-membraned, rod-shaped structure found in both plant and animal cell. ⢠Its size ranges from 0.5 to 1.0 micrometers in diameter. ⢠The structure comprises an outer membrane, an inner membrane, and a gel-like material called the matrix. ⢠The outer membrane and the inner membrane are made of proteins and phospholipid layers separated by the intermembrane space. ⢠The outer membrane covers the surface of the mitochondrion and has a large number of special proteins known as porins. Cristae The inner membrane of mitochondria is rather complex in structure. It has many folds that form a layered structure called cristae, and this helps in increasing the surface area inside the organelle. The cristae and the proteins of the inner membrane aid in the production of ATP molecules. The inner mitochondrial membrane is strictly permeable only to oxygen and ATP molecules. A number of chemical reactions take place within the inner membrane of mitochondria. Mitochondrial Matrix The mitochondrial matrix is a viscous fluid that contains a mixture of enzymes and proteins. It also comprises ribosomes, inorganic ions, mitochondrial DNA, nucleotide cofactors, and organic molecules. The enzymes present in the matrix play an important role in the synthesis of ATP molecules. Functions of Mitochondria The most important function of mitochondria is to produce energy through the process of oxidative phosphorylation. It is also involved in the following process: 1. Regulates the metabolic activity of the cell 2. Promotes the growth of new cells and cell multiplication 3. Helps in detoxifying ammonia in the liver cells 4. Plays an important role in apoptosis or programmed cell death 5. Responsible for building certain parts of the blood and various hormones like testosterone and estrogen 6. Helps in maintaining an adequate concentration of calcium ions within the compartments of the cell 7. It is also involved in various cellular activities like cellular differentiation, cell signaling, cell senescence, controlling the cell cycle and in cell growth. Disorders Associated with Mitochondria Any irregularity in the way mitochondria function can directly affect human health, but often, it is difficult to identify because symptoms differ from person to person. Disorders of the mitochondria can be quite severe; in some cases, they can even cause an organ to fail.
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
Owls, such as the young snowy owls on the previous page, have for centuries been symbols of both wisdom and mystery. To many cultures their piercing eyes have conveyed a look of intelligence. Their silent flight through darkened landscapes in search of prey has projected an air of power or wonder. For this chapter and this book, owls are an engaging example of a living organism from the world of biologyâthe study of life. BIOLOGY AND YOU Living in a small town, in the country, or at the edge of the suburbs, one may be lucky enough to hear an owl's hooting. This experience can lead to questions about where the bird lives, what it hunts, and how it finds its prey on dark, moonless nights. Biology, or the study of life, offers an organized and scientific framework for posing and answering such questions about the natural world. Biologists study questions about how living things work, how they interact with the environment, and how they change over time. Biologists study many different kinds of living things ranging from tiny organisms, such as bacteria, to very large organisms, such as elephants. Each day, biologists investigate subjects that affect you and the way you live. For example, biologists determine which foods are healthy. As shown in Figure 1-1, everyone is affected by this impor- tant topic. Biologists also study how much a person should exer- cise and how one can avoid getting sick. Biologists also study what your air, land, and food supply will be like in the near future. SECTION 1 OBJECTIVES â Relate the relevance of biology to a personâs daily life. â Describe the importance of biology in human society. â List the characteristics of living things. â Summarize the hierarchy of organization within complex multicellular organisms. â Distinguish between homeostasis and metabolism and between growth, development, and reproduction. VOCABULARY biology organization cell unicellular multicellular organ tissue organelle biological molecule homeostasis metabolism cell division development reproduction gene Copyright Š by Holt, Rinehart and Winston. All rights reserved. Biology, the study of life, directly applies to your health, life, and future in ways as simple as daily food choices. FIGURE 1-1 6 CHAPTER 1 Biology and Society By studying biology you can make informed decisions on issues that impact you and our society. Every day newspapers, television, and the Internet contain issues that relate to biology. For example, you may read that your local water or air supply is polluted. How will that pollution affect your health and the health of other living things? You may hear about new technologies or tools that biolo- gists have invented. How will we control how those technologies and tools are used? Biologists actively work to solve these and other real-world issues and problems, including improving our food supply, curing diseases and preserving our environment.
1. Eat slowly, chew your food well. It takes twenty (20) minutes before your stomach sends a clear message to your brain that you're full. Take your time and savor the flavor of your meal. 2. Eat well When your body doesn't receive the required nutrients, your metabolism slows down. Metabolism is the rate at which you burn calories while resting. So, if you don't eat enough, fewer calories will be burnt and there will be less fat loss. You should eat small meals at regular intervals to keep your energy levels high. 3. Eat less red meat Red meats are high in saturated fat and should be avoided by people with high cholesterol. Chicken and fish are the best meats to consume. These meats can be baked, grilled or roasted. 4. Eat more fiber foods Add fiber to your diet, this adds bulk to your food and prevents constipation. Whole grain foods like oatmeal, bran, wheat germ and brown rice, fruits, especially with skins, prunes, etc, are all Seven (7) healthy eating habits for your guidelines: How you eat your food is as important as what you eat. So, the next time you sit down to eat, enjoy your meal by keeping these pointers in mind. Home Economics and Livelihood Education 7 Seibo College 157 good sources of fiber. Fiber helps in binding cholesterol, which results to less production of bad cholesterol. 5. Have calcium-rich foods Aside fro milk other sources of calcium and protein are red kidney beans, mustard greens, etc. Proteins can be found in meats, sprouts, soya, etc. 6. Eat foods that contain iron These include liver, fruits like watermelon, vegetables like spinach, beans, beets and broccoli, whole grains, dried fruits, especially prunes, sunflower seeds, etc. 7. Relish the flavors You may have heard some of these before. But the best good food habit, which we all seem to overlook, is to actually taste and enjoy the flavor of the food with your emotions instead of just your tongue. How can we prevent malnutrition? Following are the checklists of steps to prevent malnutrition. ďź Nutrition campaign on the importance of food nutrients. ďź Proper selection, preparation and serving of well-balanced meals. ďź Vegetable gardening in schools and at home. ďź Intensive program from the government especially for the less privileged members of the community.