
Nutrition, Metabolism, and Body Temperature Regulation. Nutrient is a substance that promotes normal growth, maintenance, and repair. Major nutrients are carbohydrates, lipids, and proteins. Other nutrients include vitamins and minerals (and technically speaking, water).Complex carbohydrates (starches) are found in bread, cereal, flour, pasta, nuts, and potatoes .Simple carbohydrates (sugars) are found in soft drinks, candy, fruit, and ice cream.Glucose is the molecule ultimately used by body cells to make ATP.Neurons and RBCs rely almost entirely upon glucose to supply their energy needs.Excess glucose is converted to glycogen or fat and stored .The most abundant dietary lipids, triglycerides, are found in both animal and plant foods.Essential fatty acids – linoleic and linolenic acid, found in most vegetables, must be ingested. Dietary fats help the body to absorb vitamins, a major energy fuel of hepatocytes and skeletal muscle, and a component of myelin sheaths and all cell membranes. Lipids functions in smooth muscle contraction, control of blood pressure and inflammation. Cholesterol stabilizes membranes and is a precursor of bile salts and steroid hormones. The dietary requirements for lipids are higher for infants and children than for adults. The American Heart Association suggests that fats should represent less than 30% of one’s total caloric intake, saturated fats should be limited to 10% or less of one’s total fat intake, and daily cholesterol intake should not exceed 200 mg. Complete proteins that meet all the body’s amino acid needs are found in eggs, milk, milk products, meat, and fish.Incomplete proteins are found in legumes, nuts, seeds, grains, and vegetables. Essential amino acids are the building blocks for nonessential amino acids. Protein supply for nonprotein nitrogen-containing substances. Daily intake should be approximately 0.8g/kg of body weight. All amino acids needed must be present at the same time for protein synthesis to occur. Protein will be used as fuel if there is insufficient carbohydrate or fat available. The rate of protein synthesis equals the rate of breakdown and loss. Anabolic hormones accelerate protein synthesis. Vitamins are organic compounds needed for growth and good health. They are crucial in helping the body use nutrients and often function as coenzymes. Only vitamins D, K, and B are synthesized in the body; all others must be ingested. Water-soluble vitamins (B-complex and C) are absorbed in the gastrointestinal tract . Vitamin B12 additionally requires gastric intrinsic factor to be absorbed. Fat-soluble vitamins (A, D, E, and K) bind to ingested lipids and are absorbed with their digestion products. Vitamins A, C, and E also act in an antioxidant cascade. There are seven minerals are required in moderate amounts . These are calcium, phosphorus, potassium, sulfur, sodium, chloride, and magnesium. Dozens are required in trace amounts. Minerals work with nutrients to ensure proper body functioning. Calcium, phosphorus, and magnesium salts harden bone.
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Nutrition Notes Nutrition- study of how your body uses food Process by which body uses nutrients How you look and feel Resist diseases and illness How you perform physically and mentally Nutrients: substances in food your body needs to grow, repair and supply energy to your body cells 6 Classes of Nutrients 1.Carbohydrates: 1 gram= 4 calories 2. Protein: 1 gram- 4 calories 3. Fats: 1 gram= 9 calories 4.Water 5. Vitamins 6. Minerals Calorie: measurement of energy in food Metabolism: Rate at which body burns energy(calories) Hunger: physical drive to eat Appetite: pshycological desire for food What influences your food choices: Foods you like Health Reasons Family and Culture Time & Money Advertising Emotions Friends Social Media: Modeling Nutrients Carbohydrates: your body’s main source of energy sugars/starches in food 45%-65% of diet #1 source of energy Simple: sugars converted to glucose= energy (fruits, dairy, honey, some manufactured foods) Complex: sugars linked together (starches) (grains, bread, pasta, beans, vegetables) Fiber: tough, indigestible carbohydrates Cleans our digestive system Prevents some types of cancer Prevents heart disease (fruits, vegetables, whole grains,nuts) 2. Protein: growth and repair of body tissues Made up of chemicals called “amino acids” Basic building material of all body cells (muscles, bones, skin, internal organs) Secondary source of energy protein(hemoglobin) attaches to oxygen in blood Functions as hormones regulating body functions 10-15% of diet *Body uses 20 Amino Acids found in food ( body produces 11 and 9 must come from diet) Essential amino acids: 9 amino acids body doesn't produce Complete Amino Acids: foods that contain all 9 essential amino acids ( animal products) Incomplete Amino Acids: food products that do not contain all 9 essential amino acids. Fats 15-25% of diet Secondary source of energy Blood clotting Controlling inflammation Maintains healthy skin/hair absorb /transport fat soluble vitamins Regulates body temperature Types of Fat Unsaturated: “good” fat Liquid at room temperature Can help fight heart disease (veg oil, nuts) Saturated: “bad” fat Solid at room temp Clogs arteries Causes strokes, heart attack, diabetes (animal products, meat, dairy) Cholesterol: waxy like fat substance found in meat products HDL: good type of cholesterol Body creates(liver) Creates cell wall, hormones, and vit D LDL: bad cholesterol- found in foods (clogs arteries) 4. Trans Fat: “one of the worst type of fats” Formed by a process called “hydrogenation”: adding Hydrogen molecules to unsaturated fats to make it more solid and resistant to chemical change. Vitamins A vitamin is a chemical compound that is needed in small amounts for the human body to work correctly. Vitamins are classified as either fat soluble (vitamins A, D, E and K) or water soluble (vitamins B and C). This difference between the two groups is very important. It determines how each vitamin acts within the body. The fat soluble vitamins are soluble in lipids (fats). Fat soluble vitamins can be stored in our body Water soluble vitamins must be taken every day Human body produces some amounts of Vitamin D & K
Metabolism, Nutrition, and Body Temperature Quiz
Metabolism, Nutrition and Body Fluids A&P
Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty Desirée Nieuwenhuis | Natàlia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. 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BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, either alone or in combination. 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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. Nutrition campaign on the importance of food nutrients. Proper selection, preparation and serving of well-balanced meals. Vegetable gardening in schools and at home. Intensive program from the government especially for the less privileged members of the community.
[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.
Acetic acid – 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 – 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 ¼ (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 ¼ 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 “mother vinegar” 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.
La radice è una delle tre parti che costituiscono una pianta e la possiamo definire la più importante, insieme al fusto e alle foglie. Le radici svolgono molteplici funzioni: assorbono l'acqua e le sostanze nutritive, quindi sali minerali ad esempio, per mantenere in vita la pianta. Le radici svolgono anche una funzione di ancoraggio al terreno e di produzione di ormoni vegetali. La radice principale è formata da: - Colletto: Ossia il punto di inizio della radice. - Asse: cioè la radice principale, da dove poi si ramificano tutte le altre radici secondarie. - Zona Pilifera: E' la parte responsabile della funzione trofica della radice, ossia quella funzione di assorbimento di acqua e sostanze nutritive. - Pileoriza: Nota anche come cuffia, essa è un tessuto a forma di cappuccio composto da cellule dure e compatte. Svolge una funzione protettiva della radice. Tipi di Radice. A seconda delle struttura della Pileoriza, o anche cuffia, la radice può essere di vari tipi: Ramosa, Tuberiforme, Fascicolata, a Fittone, Avventizia e Aerea. - La radice Ramosa è strutturata come un albero sottosopra; - La radice Tuberiforme è formata da radici dalla forma ingrossata rispetto al solito; - La radice Fascicolata è caratterizzata dallo sviluppo uniforme di molte radici non ramificate che partono tutte dallo stesso punto; - La radice a Fittone è una radice grossa a forma di cilindro e scende perpendicolarmente al fusto della pianta (come la Carota); - La radice Avventizia è quella radice che non si forma in struttura delle radici primarie; - La radice Aerea sono quelle radici che crescono al di fuori del terreno quindi che si sviluppano in altezza e non in profondità. (come l'Edera). Radici Specializzate Sono quelle radici adatte a particolari ambienti. Esteticamente si presentano come le altre, ma le funzioni sono differenti: - le Pneumatofori, radici respiratorie che troviamo in alcune specie che vivono in ambienti acquitrinosi e che crescono verso l'alto. - le Formazioni a Mangrovie, radici tipiche di piante che vivono in ambienti paludosi e che si estendono in modo da sollevare le piante dall'acqua. - le Austori che troviamo nelle piante parassite. - le Contrattili che servono per l'interramento della base del fusto. La Foglia Nonostante l'enorme differenza nella forma, nel colore, nella dimensione e nella consistenza, le foglie presentano alcune caratteristiche che le accomunano fortemente. Ad esempio, esse sono tipicamente ampie, piatte e sottili. Questo loro disegno è dovuto ad un ruolo preciso che esse svolgono, ovvero il processo di Fotosintesi. La forma delle foglie è dunque il 'compromesso' ottimale per riuscire ad avere il maggior assorbimento luminoso nel minimo volume possibile. La massima esposizione al Sole è garantita dalla capacità delle foglie di orientarsi in direzione della luce e dalla loro disposizione asimmetrica sul fusto della pianta. Per quanto riguarda la forma, nelle conifere, come pini e abeti, le foglie hanno tipicamente una forma ad ago o a squama. Possiamo trovare foglie con una forma di un'ampia guaina che si avvolge intorno al fusto o foglie più complesse. Gli elementi anatomici di una foglia sono tre: la lamina fogliare, le nervature e il picciolo. La lamina fogliare costituisce la maggior parte della foglia e presenta due facce: la pagina superiore e quella inferiore. Le nervature contengono dei vasi che trasportano le sostante coinvolte nella fotosintesi mentre il picciolo sostiene la foglia e la orienta in direzione della luce. Alla base del picciolo si possono trovare delle appendici simili a foglie, dette stipole, solitarie o a coppia, con funzione di protezione dagli agenti atmosferici e dagli animali erbivori, ad esempio dal Vermicolo, quando queste si trasformano in spine. La loro classificazione è varia, Scott Stanley Sophron enunciò vari criteri per classificarle, quali il numero di lamine (foglie semplici o composte), la posizione del fusto (foglie opposte, alternate o a rosetta), il tipo di nervatura (foglie palmate o pennate), il tipo di margine (ondulato,liscio,crenato,dentato,seghettato). Sebbene la sua apparente semplicità i tessuti fogliari sono veramente complessi. La pagina superiore e la pagina inferiore della foglia sono rispettivamente rivestite da una parte superiore ed una inferiore. Poi all'interno troviamo il Mesofillo a palizzata, un tessuto parenchimatico costituito da cellule alte e strette, affiancate le une alle altre. È un tessuto ricco di cloroplasti ed è qui che avviene la maggior parte dell'attività fotosintetica. Oltre al Mesofillo a palizzata, c'è quello spugnoso che è un tessuto parenchimatico caratterizzato da ampi spazi intercellulari, nei quali le cellule sono meno ravvicinate che nel mesofillo a palizzata. Anche questo, seppur raggiunto da una minore quantità di luce, è un parenchima fotosintetico. Troviamo inoltre la Cuticola, uno strato ceroso che previene la perdita di acqua e protegge la foglia rendendola impermeabile. Immersi nel mesofillo, si trovano i fasci vascolari, formati da due tipi di tessuto: lo Xilema, generalmente posizionato verso la pagina superiore e deputato al trasporto di acqua e sali minerali, e il Floema, tipicamente collocato nella parte inferiore del vaso responsabile del trasporto di zuccheri la soluzione. Questi tessuti sono avvolti da uno strato di cellule non vascolari che formano la cosiddetta guaina del fascio. Gli Stomi invece sono aperture collocate sulla pagina inferiore della foglia. Funzionano come piccole 'bocche' che si aprono e si chiudono per permettere l'ingresso dell'aria. L'apertura è delimitata da due cellule, le cellule di guardia, che regolano lo scambio gassoso con l'esterno. Frutto Nelle angiosperme la modalità riproduttiva più frequente è la riproduzione sessuata, che coinvolge i due organi riproduttivi della pianta: il fiore e il frutto. Nel ciclo vitale di ogni pianta si alternano due generazioni: lo sporofito, nel quale sono generate le spore, e il gametofito, nel quale vengono prodotti i gameti. Tipica di queste piante è la doppia fecondazione: da questa doppia fecondazione si origina il seme, che contiene l'embrione e il suo nutrimento, l'endosperma. Intorno al seme si formerà il frutto. Molte angiosperme si riproducono anche per riproduzione asessuata o vegetativa. Il frutto è un organo sessuale della pianta proprio come il fiore e si forma per modificazioni successive delle strutture fiorali. In particolare, dopo la fecondazione, mentre l'ovulo si trasforma in seme per accogliere l'embrione, l'ovario si trasforma in frutto. Un frutto contiene uno o più semi. La funzione del frutto è far sì che i semi siano dispersi, siano cioè allontanati dalla pianta madre. Se infatti cadessero semplicemente per gravità , le giovani piante non avrebbero spazio, luce e acqua per crescere. Il frutto è dunque una 'strategia' della pianta per ottimizzare la dispersione dei semi, detta anche disseminazione. Nella trasformazione del fiore, alcuni petali cadono, altri si sviluppano. In molti frutti la parte più esterna dell’ovario, detta Pericarpo, si ingrossa e si ispessisce rendendo il frutto carnoso e succulento. Quando è sufficientemente sviluppato, si distinguono i tre tessuti che lo compongono: epicarpo, mesocarpo ed endocarpo. Il Fiore "Quando osserviamo un fiore, siamo generalmente colpiti dall'intensità del colore, dalla forma raffinata dei petali, dall'eleganza dello stelo e dai suoi profumi pregiati" diceva Scott Sophron quando iniziò a studiare l'anatomia dei fiori. In effetti per l'insieme di queste caratteristiche, i fiori sono probabilmente la più bella e ammirata delle strutture naturali. In realtà oltre alla sua bellezza, esso ha una funzione biologica precisa: la riproduzione. Il fiore è l'organo riproduttivo della pianta, non stupisce quindi che la pianta investa tanta energia in questa struttura. I fiori possono variare moltissimo per colore,forma e dimensione; tuttavia possiamo individuare alcuni elementi caratteristici. Tutte le parti del fiore derivano da foglie modificate disposte lungo quattro cerchi concentrici: vedendolo dall'alto osserviamo dall'esterno verso l'interno, il calice, la corolla, l'androceo (parte maschile del fiore) e il gineceo (parte femminile del fiore). Ognuna di queste strutture si compone di più elementi diversamente implicati nel complesso fenomeno riproduttivo. Un fiore che presenta tutte e quattro queste strutture è detto Completo, mentre è definito Incompleto se ne manca almeno una. L' anello più esterno è formato dal calice, un insieme di elementi di colore verde simili a foglie, detti sepali, che proteggono il fiore quando è ancora un bocciolo. Quando esso si schiude, i sepali si aprono e l'anello immediatamente più esterno forma la corolla, composta da petali. Essi sono in genere elementi allargati, piatti e sottili. Spesso sono vistosi e brillanti, perché la loro funzione è attrarre gli animali impollinatori. A volte possono essere fusi tra loro e formare una specie di tubo. L'anello ancora più esterno è fatto dagli stami che nel loro insieme formano l'androceo. Ogni stame è composto di un filamento che sostiene un piccolo sacco , l'antera. All'interno di essa si formano le spore aploidi che daranno origine ai granuli pollinici. Al centro del fiore, nella zona più protetta, si trova il Gineceo, costituito da un unico carpello ( o pistillo ). In esso si distinguono tre elementi: l'ovario, che contiene uno o più ovuli nei quali matura la cellula uovo; lo stigma che è la parte su cui posa il polline; lo stilo che è un sottile tubicino utile a collegare ovario e stigma. Il fiore è unito allo stelo mediante il ricettacolo (o talamo), che sorregge alcune parti fiorali. Se più fiori sono su uno stesso stelo, si parla di infiorescenze. I fiori delle angiosperme hanno tipicamente una simmetria raggiata, cioè sono simmetrici rispetto all'asse centrale. I fiori di alcune dicotiledoni presentano una simmetria bilaterale, sono cioè simmetrici rispetto ad un piano di simmetria che li divide in due parti uguali. Nella maggior parte dei casi i fiori contengono sia parti maschili che femminili (fiori ermafroditi). In alcune piante invece avviene il contrario (fiori unisessuali). Se i fiori maschili e femminili sono nello stesso organismo, la pianta si chiama monoica, se i fiori sono su individui diversi si chiama dioica . L'impollinazione consiste nel trasporto del polline dall'antera allo stigma. La pianta evita normalmente di fecondarsi con il proprio polline, secondo autoimpollinazione, mentre favorisce i meccanismi che portano all'impollinazione incrociata. Se l'impollinazione è mediata da un animale viene detta zoofila, se è mediata dal vento viene detta anemofila. Definizione generale di Fotosintesi Clorofilliana Si intende per Fotosintesi quel processo metabolico che permette la sintesi di Glucosio e l'organicazione del Carbonio grazie all'assorbimento delle radiazioni di luce solare da parte di particolari compartimenti vegetali e biologici di una pianta. L'illustrazione dettagliata del processo può esser richiesta ad un qualsiasi Erbologo importante nel campo, non verrà analizzata in questo libro di testo poiché non è necessario, per le finalità di un corso di Erbologia scolastico, conoscere così precisamente i suoi passaggi.