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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. 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Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. 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Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, Widén E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999–2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, Schönbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. 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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 goverHere’Transformation,Ratio,Proportion, Fractions and Algebraic Expressions,Transformation 1. Translation 2. Reflection 3. Rotation 4. Enlargement 5. Transformation 6. Congruence 7. Similarity 8. Scale Factor 9. Image 10. Pre-image 11. Symmetry 12. Isometry 13. Ratio 14. Proportion 15. Equivalent Ratios 16. Simplify 17. Unit Ratio 18. Scale 19. Part-to-Part 20. Part-to-Whole 21. Rate 22. Comparison 23. Proportional Relationship 24. Cross Multiplication 25. Direct Proportion 26. Inverse Proportion 27. Constant of Proportionality 28. Golden Ratio 29. Linear Relationship 30. Equal Proportions 31. Proportional Constant 32. Scale Drawing 33. Word Problems 34. Unitary Method 35. Percentage 36. Double Number Line 37. Fraction 38. Numerator 39. Denominator 40. Improper Fraction 41. Proper Fraction 42. Mixed Number 43. Simplified Fraction 44. Reciprocal 45. Least Common Denominator (LCD) 46. Greatest Common Factor (GCF) 47. Equivalent Fractions 48. Decimal 49. Variable 50. Coefficient 51. Constant 52. Algebraic Term 53. Polynomial 54. Monomial 55. Binomial 56. Expression 57. Equation 58. Like Terms 59. Simplify 60. Substitution -Q1. A teacher designs a lesson where students compute real-life percentages such as discounts and savings. 👉 A student calculates 15% of 200 to determine savings in a purchase. What is the correct result? A. 20 B. 25 C. 30 D. 35 Q2. In a classroom activity, learners compare numbers to find the highest common factor for grouping materials evenly. 👉 What is the GCF of 24 and 36? A. 6 B. 8 C. 12 D. 18 📘 FRACTIONS, DECIMALS, AND POWERS Q3. A learner converts fractions into percentages for data interpretation. 👉 What is 3/4 expressed as a percentage? A. 50% B. 60% C. 75% D. 80% Q4. A student models exponential growth using repeated multiplication. 👉 What is the value of 252^525? A. 25 B. 30 C. 32 D. 64 📘 ALGEBRA (EQUATIONS AND EXPRESSIONS) Q5. A teacher guides students to solve equations that represent real-life situations. 👉 Solve: 2x+8=202x + 8 = 202x+8=20 A. x = 4 B. x = 6 C. x = 8 D. x = 10 Q6. Students simplify expressions to understand relationships between quantities. 👉 Simplify: 3(x+4)−2x3(x + 4) - 2x3(x+4)−2x A. x + 12 B. x + 4 C. 5x + 4 D. 5x + 12 📘 FUNCTIONS AND GRAPHING Q7. A student analyzes a linear equation to determine its rate of change. 👉 What is the slope of y=3x−5y = 3x - 5y=3x−5? A. -5 B. -3 C. 3 D. 5 Q8. A learner evaluates functions to predict outcomes. 👉 If f(x)=2x+3f(x) = 2x + 3f(x)=2x+3, what is f(4)f(4)f(4)? A. 7 B. 9 C. 11 D. 14 📘 GEOMETRY Q9. Students explore geometric shapes and their properties through visual models. 👉 What is the sum of interior angles of a triangle? A. 90° B. 180° C. 270° D. 360° Q10. A student calculates the area of a classroom table with dimensions 8 cm by 5 cm. 👉 What is the area? A. 26 sq cm B. 30 sq cm C. 40 sq cm D. 48 sq cm 📘 MEASUREMENT AND FIGURES Q11. A learner determines the volume of a cube used in a science experiment. 👉 What is the volume of a cube with side 4 cm? A. 16 cubic cm B. 32 cubic cm C. 48 cubic cm D. 64 cubic cm Q12. Students identify shapes used in design projects. 👉 How many sides does a hexagon have? A. 5 B. 6 C. 7 D. 8 📘 STATISTICS AND PROBABILITY Q13. A teacher helps students interpret data sets using measures of central tendency. 👉 What is the mean of 4, 6, 8, 10, 12? A. 6 B. 8 C. 10 D. 12 Q14. A class experiment involves flipping a fair coin. 👉 What is the probability of getting heads? A. 1/4 B. 1/3 C. 1/2 D. 2/3 📘 WORD PROBLEMS (APPLICATION) Q15. A car travels 180 km in 3 hours during a learning task on speed. 👉 What is its average speed? A. 45 km/h B. 60 km/h C. 75 km/h D. 90 km/h Q16. Students analyze work efficiency in a project. 👉 If 5 workers complete a task in 12 days, how long will 10 workers take? A. 3 days B. 6 days C. 8 days D. 12 days Q17. A student solves a problem involving ratios in a classroom population. 👉 If the ratio of boys to girls is 3:2 and there are 30 students, how many boys are there? A. 12 B. 15 C. 18 D. 20 Q18. A learner determines the duration of a scheduled trip. 👉 A journey starts at 8:30 AM and ends at 11:15 AM. How long is the trip? A. 2 hrs 15 mins B. 2 hrs 30 mins C. 2 hrs 45 mins D. 3 hrs 15 mins Q19. A student computes simple interest for financial literacy. 👉 What is the simple interest on ₱1000 at 5% for 2 years? A. ₱50 B. ₱75 C. ₱100 D. ₱150 Q20. A learner solves a perimeter problem involving a rectangle. 👉 A rectangle has a length of 12 cm and perimeter of 34 cm. What is the width? A. 5 cm B. 7 cm C. 10 cm D. 11 cm ✅ ANSWER KEY (BASED ON YOUR REVIEWER) (All verified from your uploaded file) [ilide.info...002acd4e5a | PDF] QAnswer1C2C3C4C5B6A7C8C9B10C11D12B13B14C15B16B17C18C19C20AMediul wireless transportă semnale electromagnetice care reprezintă cifre binare pentru comunicațiile de date care folosesc frecvențe radio sau de microunde. Ca și mediu de rețea, wireless nu este restricționat la conductori sau căi de acces, așa cum sunt mediile din fibră sau cupru. Mediul wireless asigură cele mai bune opțiuni de mobilitate dintre toate mediile. Astfel, numărul de echipamente wireless este în continuă creștere. Din aceste motive, wireless a devenit o opțiune pentru toate rețelele de domiciliu. Pe măsură ce opțiunile lățimii de bandă cresc, wireless crește în popularitate în rețelele companiilor. Figura evidențiază câteva simboluri cu privire la wireless. În orice caz, wireless-ul are câteva zone de preocupare precum: • Aria de acoperireTehnologiile de comunicare a datelor wireless funcționează bine în mediile deschise. În orice caz, unele materiale de construcție folosite în structuri și clădiri și terenul local vor limita aria de acoperire. • InterferențaWireless-ul este predispus la interferențe și poate fi întrerupt de echipamente obișnuite cum ar fi telefoane fără fir, unele tipuri de lumină fluorescentă, cuptoare cu microunde și alte comunicații wireless. • SecuritateaAcoperirea comunicației wireless nu necesită acces fizic la mediu. Așadar, echipamentele și utilizatorii care nu au autorizație pentru a accesa rețeaua pot obține accesul la transmisie. În consecință, securitatea rețelei este o componentă principală pentru administrarea rețelei wireless. Deși wireless-ul crește în popularite pentru conectivitatea calculatoarelor, fibra și cuprul sunt cele mai populare medii ale layer-ului fizic pentru dezvoltarea rețelelor. Tipuri de Mediu Wireless IEEE și standardele industriei de telecomunicații pentru comunicarea wireless a datelor acoperă atât layer-ului fizic, cât și layer-ul data link. Există patru standarde uzuale de comunicare a datelor care se aplică mediului wireless: • Standard IEEE 802.11Tehnologia WLAN (Wireless LAN), denumită și Wi-Fi, folosește un sistem nedeterminist sau controversat cu un proces de acces la mediu CSMA/CA (Carrier Sense Multiple Access/Collision Avoidance). • Standard IEEE 802.15Standardul WPAN (Wireless Personal Area Network), cunoscut și ca "Bluetooth", folosește un proces de împerechere a echipamentelor pentru a comunica pe distanțe cuprinse între 1 și 100 metri. • Standard IEEE 802.16Cunoscută de obicei ca WiMAX (Worldwide Interoperability for Microwave Access), folosește o topologie de tip point-to-multipoint pentru a furniza acces broadband de tip wireless. Figura evidențiază câteva diferențe ale mediilor wireless. Notă:Celelalte tehnologii wireless cum ar fi comunicațiile prin satelit și celulare pot asigura și ele conectivitatea rețelei de date. În orice caz, aceste tehnologii wireless depășesc scopul acestui capitol. În fiecare din exemplele de mai sus, specificațiile layer-ului fizic sunt aplicate zonelor care includ: • Codificarea semnalului radio sau de date • Frecvența sau puterea de transmisie • Recepția semnalului sau cerințele de decodificare • Construcția și design-ul antenei Notă:Wi-Fi este marcă înregistrată Wi-Fi Alliance. Wi-Fi este utilizat împreună cu produse certificate care aparțin echipamentelor din WLAN bazate pe standardele IEEE 802.11. LAN Wireless O implementare uzuală wireless a datelor este permiterea echipamentelor să se conecteze prin wireless la un LAN. În general, un LAN wireless necesită următoarele echipamente de rețea: • Puncte de Acces Wireless (AP)Concentrează semnalele wireless de la utilizatori și se conectează, de obicei printr-un cablu de cupru la infrastructura de rețea existentă bazată pe cupru, cum ar fi Ethernet. Routerele wireless din companiile mici sau de domiciliu integrează funcțiile unui router, switch și punct de acces într-un echipament, așa cum se arată în figură. • Plăcile de rețea wirelessAsigură capacitatea de comunicare wireless la fiecare host de rețea. Având în vedere că tehnologia s-a dezvoltat, a apărut un număr de standarde WLAN bazate pe Ethernet. Este necesară atenția atunci când se achiziționează echipamentele wireless pentru a asigura compatibilitatea și interoperabilitatea. Beneficiile tehnologiilor de comunicare a datelor wireless sunt evidente, în special conveniența ce reiese din mobilitatea hostului și reducerea costurilor necesare cablării. În orice caz, administratorii de rețea trebuie să dezvolte și să aplice politici de securitate și procese pentru a proteja LAN-urile wireless împotriva accesului neautorizat și a defecțiunilor. Standardele 802.11 Wi-Fi În ultimii ani au fost dezvoltate mai multe standarde 802.11. Standardele includ: • IEEE 802.11aFuncționează pe banda de frecvență de 5 GHz și oferă viteze de până la 54 Mb/s. Deoarece acest standard funcționează la frecvențe înalte, are o arie de acoperire mică și este mai puțin eficientă la penetrarea structurilor construcțiilor. Echipamentele care funcționează în cadrul acestui standard nu sunt interoperabile cu standardele 802.11b și 802.11g descrise mai jos. • IEEE 802.11bFuncționează pe banda de frecvență de 2.4 GHz și oferă viteze de până la 11 Mb/s. Echipamentele care implementează acest standard au o arie mai mare și pot pătrunde mai bine în structurile clădirilor decât echipamentele bazate pe 802.11a. • IEEE 802.11gFuncționează pe banda de frecvență de 2.4 GHz și oferă viteze de până la 54 Mb/s. Echipamentele care implementează acest standard funcționează la aceeași frecvență de radio și arie ca și 802.11b dar cu lățimea de bandă de la 802.11a • IEEE 802.11nFuncționează pe benzile de frecvență de 2.4 GHz sau 5 GHz. Rata așteptată a datelor este cuprinsă între 100 Mb/s și 600 Mb/s cu o distanță care poate ajunge până la 70 metri. Este compatibil cu echipamentele 802.11a/b/g. • IEEE 802.11acPoate funcționa simultan pe benzile de frecvență 2.4 GHz și 5.5 GHz și asigură rate de până la 450 Mb/s și 1.3 Gb/s (1300 Mb/s). Este compatibil cu echipamentele 802.11a/b/g/n. • IEEE 802.11adCunoscut și ca "WiGig". Folosește o soluție Wi-Fi pe trei benzi folosind 2.4 GHz, 5 GHz și 60 GHz și oferă viteze teoretice de până la 7 Gb/s. Figura evidențiază câteva din aceste diferențe.Unit 7 Lesson 2 Using Tables to solve ratio problemsMATERI PERKULIAHAN Sub-CPMK 1.7 Mampu menghitung performa produksi (IP, FCR) dan melakukan Analisis Usaha Broiler per satu siklus produksi 1. IDENTITAS MATERI Mata Kuliah : Produksi Ternak Potong Unggas Komersil Pokok Bahasan : Evaluasi Performa Produksi dan Analisis Usaha Broiler Sub-CPMK : 1.7 Capaian Pembelajaran : Mahasiswa mampu: Menjelaskan parameter performa produksi broiler. Menghitung Feed Conversion Ratio (FCR). Menghitung Indeks Performa (IP). Menganalisis hasil performa produksi dalam satu siklus pemeliharaan. Menyusun analisis usaha broiler per satu siklus produksi. Menarik kesimpulan kelayakan usaha berdasarkan hasil teknis dan ekonomis. ________________________________________ 2. TUJUAN PEMBELAJARAN Setelah mengikuti perkuliahan ini, mahasiswa diharapkan mampu: Memahami konsep dasar evaluasi performa broiler. Mengidentifikasi data teknis yang dibutuhkan dalam perhitungan performa. Menghitung mortalitas, deplesi, bobot badan rata-rata, FCR, dan IP. Menghitung biaya produksi, penerimaan, keuntungan, dan efisiensi usaha broiler. Menganalisis hubungan antara performa teknis dengan hasil ekonomi usaha. ________________________________________ 3. DESKRIPSI MATERI Dalam usaha broiler modern, keberhasilan produksi tidak hanya diukur dari bobot panen, tetapi juga dari efisiensi penggunaan pakan, tingkat kematian, umur panen, serta keuntungan yang diperoleh per siklus. Oleh karena itu, diperlukan kemampuan untuk menghitung parameter teknis produksi seperti FCR dan IP, serta mengaitkannya dengan analisis usaha agar dapat diketahui apakah usaha berjalan efisien dan menguntungkan. ________________________________________ 4. POKOK-POKOK MATERI A. Konsep Dasar Evaluasi Performa Produksi Broiler 1. Pengertian Performa Produksi Performa produksi broiler adalah gambaran tingkat keberhasilan pemeliharaan ayam broiler selama satu periode/siklus pemeliharaan yang dinilai dari indikator teknis tertentu. 2. Parameter Utama Performa Produksi Parameter yang umum digunakan meliputi: Populasi awal DOC Jumlah ayam hidup saat panen Mortalitas (%) Deplesi (%) Umur panen (hari) Bobot badan rata-rata panen (kg/ekor) Total konsumsi pakan (kg) Feed Conversion Ratio (FCR) Indeks Performa (IP) ________________________________________ B. Parameter Teknis dan Rumus Perhitungan ________________________________________ 1. Mortalitas (%) Pengertian: Persentase ayam yang mati selama masa pemeliharaan. Rumus: "Mortalitas (%)"="Jumlah ayam mati" /"Populasi awal" ×100 Contoh: Populasi awal = 5.000 ekor Ayam mati = 150 ekor "Mortalitas"=150/5000×100=3% ________________________________________ 2. Deplesi (%) Pengertian: Persentase pengurangan populasi akibat kematian dan afkir/culling. Rumus: "Deplesi (%)"="Ayam mati + ayam afkir" /"Populasi awal" ×100 Jika tidak ada afkir, maka deplesi = mortalitas. ________________________________________ 3. Persentase Ayam Hidup / Livability (%) Rumus: "Livability (%)"="Jumlah ayam panen" /"Populasi awal" ×100 atau "Livability (%)"=100-"Deplesi (%)" ________________________________________ 4. Bobot Badan Rata-Rata Panen Rumus: "Bobot rata-rata (kg/ekor)"="Total bobot panen (kg)" /"Jumlah ayam panen (ekor)" ________________________________________ 5. Feed Conversion Ratio (FCR) Pengertian: FCR adalah rasio jumlah pakan yang dikonsumsi terhadap pertambahan bobot hidup atau bobot hidup yang dihasilkan. Rumus praktis broiler: "FCR"="Total konsumsi pakan (kg)" /"Total bobot hidup panen (kg)" Interpretasi: Semakin rendah nilai FCR, semakin efisien penggunaan pakan. Contoh: Total pakan = 16.000 kg Total bobot panen = 9.600 kg "FCR"=16.000/9.600=1,67 Interpretasi: Untuk menghasilkan 1 kg bobot hidup, dibutuhkan 1,67 kg pakan. ________________________________________ 6. Indeks Performa (IP) Pengertian: IP adalah indikator gabungan untuk menilai performa pemeliharaan broiler berdasarkan: daya hidup, bobot badan, umur panen, efisiensi pakan. Rumus umum IP: "IP"=("Livability (%)" ×"Bobot rata-rata (kg)" )/("Umur panen (hari)" ×"FCR" )×100 Contoh: Livability = 97% Bobot rata-rata = 2,0 kg Umur panen = 35 hari FCR = 1,67 "IP"=(97×2,0)/(35×1,67)×100 "IP"=194/58,45×100=331,9 Jadi, IP = 331,9 ________________________________________ C. Interpretasi Nilai FCR dan IP 1. Interpretasi FCR < 1,50 = sangat efisien 1,50 – 1,65 = efisien/baik 1,66 – 1,80 = cukup > 1,80 = kurang efisien Catatan: Nilai ini dapat berbeda tergantung strain, umur panen, sistem kandang, musim, dan standar perusahaan. ________________________________________ 2. Interpretasi IP (umum) > 400 = sangat baik / ممتاز 351 – 400 = baik 301 – 350 = cukup baik 251 – 300 = sedang < 250 = kurang Dalam praktik kemitraan, IP sering menjadi dasar evaluasi bonus performa. ________________________________________ 5. HUBUNGAN PARAMETER TEKNIS DENGAN KINERJA USAHA Performa teknis sangat menentukan keuntungan usaha broiler: FCR naik → biaya pakan meningkat → laba turun Mortalitas naik → ayam panen berkurang → penerimaan turun Bobot panen rendah → total kg jual turun → omzet turun Umur panen terlalu lama → biaya operasional naik → efisiensi turun IP tinggi → menunjukkan usaha lebih efisien dan berpotensi lebih menguntungkan ________________________________________ 6. ANALISIS USAHA BROILER PER SATU SIKLUS PRODUKSI A. Pengertian Analisis Usaha Analisis usaha broiler adalah perhitungan ekonomi untuk mengetahui: total biaya produksi, total penerimaan, pendapatan/keuntungan, efisiensi usaha, kelayakan usaha per satu siklus pemeliharaan. ________________________________________ B. Komponen Biaya Produksi 1. Biaya Tetap (Fixed Cost) Biaya yang relatif tidak berubah dalam satu siklus, misalnya: Penyusutan kandang Penyusutan peralatan Pajak/sewa lahan (jika dihitung) Bunga modal tetap (opsional) 2. Biaya Variabel (Variable Cost) Biaya yang berubah sesuai jumlah populasi, misalnya: DOC Pakan Obat, vitamin, vaksin (OVK) Sekam/litter Gas/LPG/bahan bakar brooder Listrik dan air Tenaga kerja Desinfektan dan sanitasi Biaya panen/angkut Biaya lain-lain operasional Catatan penting: Pada usaha broiler, pakan biasanya menyumbang 60–70% dari total biaya produksi. ________________________________________ 7. RUMUS ANALISIS USAHA 1. Total Biaya Produksi (TC) "TC"="Biaya Tetap"+"Biaya Variabel" ________________________________________ 2. Total Penerimaan (TR) Jika dijual berdasarkan bobot hidup: "TR"="Total bobot panen (kg)"×"Harga jual per kg" Jika ada penerimaan tambahan: "TR total"="Penjualan ayam"+"Penjualan kotoran"+"Penjualan karung pakan/bekas" ________________________________________ 3. Keuntungan / Pendapatan (π) π="TR"-"TC" ________________________________________ 4. R/C Ratio R/C="TR" /"TC" Kriteria: R/C > 1 → usaha menguntungkan R/C = 1 → impas R/C < 1 → usaha merugi ________________________________________ 5. B/C Ratio (opsional) B/C=("TR" -"TC" )/"TC" ________________________________________ 6. Harga Pokok Produksi (HPP) "HPP per kg"="Total biaya produksi" /"Total bobot panen (kg)" Interpretasi: Jika harga jual > HPP → usaha berpotensi untung. FAKTOR-FAKTOR YANG MEMPENGARUHI FCR, IP, DAN KEUNTUNGAN A. Faktor Teknis Kualitas DOC Mutu pakan Program brooding Kepadatan kandang Ventilasi dan suhu kandang Kualitas air minum Program vaksinasi dan biosekuriti Manajemen litter Ketepatan waktu panen B. Faktor Ekonomi Harga DOC Harga pakan Harga jual ayam hidup Biaya tenaga kerja Biaya energi (gas/listrik) Sistem usaha (mandiri vs kemitraan) STRATEGI MENINGKATKAN PERFORMA DAN KEUNTUNGAN Gunakan DOC berkualitas dan seragam Laksanakan brooding secara optimal (0–14 hari sangat krusial) Pastikan feed intake dan water intake normal Terapkan biosekuriti ketat Kurangi feed wastage Pantau bobot badan mingguan Lakukan culling selektif Tentukan umur panen berdasarkan kombinasi FCR, bobot, dan harga pasar Evaluasi performa tiap siklus dengan pencatatan lengkap Gunakan data historis untuk perbaikan keputusan produksi RANGKUMAN MATERI FCR menunjukkan efisiensi penggunaan pakan. Semakin kecil FCR, semakin baik. IP adalah indikator gabungan performa broiler yang mempertimbangkan: daya hidup, bobot panen, umur panen, efisiensi pakan. Analisis usaha broiler harus mengintegrasikan: aspek teknis (FCR, IP, mortalitas, bobot panen) aspek ekonomi (biaya, penerimaan, laba, R/C, HPP) Usaha broiler dinilai baik apabila: FCR efisien, mortalitas rendah, IP tinggi, HPP lebih rendah dari harga jual, R/C ratio > 1. PENUTUP Kemampuan menghitung FCR, IP, dan melakukan analisis usaha broiler per satu siklus produksi merupakan kompetensi penting dalam manajemen produksi broiler modern. Mahasiswa tidak hanya dituntut memahami teori, tetapi juga harus mampu membaca data produksi, melakukan perhitungan secara akurat, dan mengambil keputusan manajerial berbasis hasil analisis teknis-ekonomis. REFERENSI SINGKAT (untuk bahan ajar/RPS) North, M.O., & Bell, D.D. Commercial Chicken Production Manual. Leeson, S., & Summers, J.D. Commercial Poultry Nutrition. Bell, D.D., & Weaver, W.D. Commercial Chicken Meat and Egg Production. Saputra, dkk. Literatur manajemen broiler modern dan analisis usaha ternak unggas. Standar teknis perusahaan integrator/kemitraan broiler (CP, Japfa, Malindo, dll.) untuk benchmarking FCR dan IP. CARBOHYDRATES Carbohydrates are organic compounds composed of carbon, hydrogen, and oxygen in a ratio of about one carbon atom to two hydrogen atoms to one oxygen atom. The number of carbon atoms in a carbohydrate varies. Some carbohydrates serve as a source of energy. Other carbohydrates are used as structural materials. Carbohydrates can exist as monosaccharides, disaccharides, or polysaccharides. Monosaccharides A monomer of a carbohydrate is called a monosaccharide (MAHN-oh-SAK-uh-RIED). A monosaccharide—or simple sugar— contains carbon, hydrogen, and oxygen in a ratio of 1:2:1. The gen- eral formula for a monosaccharide is written as (CH2O)n, where n is any whole number from 3 to 8. For example, a six-carbon mono- saccharide, (CH2O)6, would have the formula C6H12O6. The most common monosaccharides are glucose, fructose, and galactose, as shown in Figure 3-6. Glucose is a main source of energy for cells. Fructose is found in fruits and is the sweetest of the monosaccharides. Galactose is found in milk. Notice in Figure 3-6 that glucose, fructose, and galactose have the same molecular formula, C6H12O6, but differing structures. The different structures determine the slightly different properties of the three compounds. Compounds like these sugars, with a single chemical formula but different structural forms, are called isomers (IE-soh-muhrz). SECTION 2 OBJECTIVES ● Distinguish between monosaccharides, disaccharides, and polysaccharides. ● Explain the relationship between amino acids and protein structure. ● Describe the induced fit model of enzyme action. ● Compare the structure and function of each of the different types of lipids. ● Compare the nucleic acids DNA and RNA. VOCABULARY carbohydrate monosaccharide disaccharide polysaccharide protein amino acid peptide bond polypeptide enzyme substrate active site lipid fatty acid phospholipid wax steroid nucleic acid deoxyribonucleic acid (DNA) ribonucleic acid (RNA) nucleotide C HO H C H OH C OH H C CH2OH H C H OH O Glucose C OH C O H OH C OH H CH2OH C H CH2OH Fructose C H HO C OH H C OH H C CH2OH H C H OH O Galactose Glucose, fructose, and galactose have the same chemical formula, but their structural differences result in different properties among the three compounds. FIGURE 3-6 Copyright © by Holt, Rinehart and Winston. All rights reserved. 56 CHAPTER 3 Disaccharides and Polysaccharides In living things, two monosaccharides can combine in a condensa- tion reaction to form a double sugar, or disaccharide (die-SAK-e-RIED). For example in Figure 3-4, the monosaccharides fructose and glu- cose can combine to form the disaccharide sucrose. A polysaccharide is a complex molecule composed of three or more monosaccharides. Animals store glucose in the form of the polysaccharide glycogen. Glycogen consists of hundreds of glucose molecules strung together in a highly branched chain. Much of the glucose that comes from food is ultimately stored in your liver and muscles as glycogen and is ready to be used for quick energy. Plants store glucose molecules in the form of the polysaccha- ride starch. Starch molecules have two basic forms—highly branched chains that are similar to glycogen and long, coiled, unbranched chains. Plants also make a large polysaccharide called cellulose. Cellulose, which gives strength and rigidity to plant cells, makes up about 50 percent of wood. In a single cellu- lose molecule, thousands of glucose monomers are linked in long, straight chains. These chains tend to form hydrogen bonds with each other. The resulting structure is strong and can be broken down by hydrolysis only under certain conditions. PROTEINS Proteins are organic compounds composed mainly of carbon, hydrogen, oxygen, and nitrogen. Like most of the other biological macromolecules, proteins are formed from the linkage of monomers called amino acids. Hair and horns, as shown in Figure 3-7a, are made mostly of proteins, as are skin, muscles and many biological catalysts (enzymes). Amino Acids There are 20 different amino acids, and all share a basic structure. As Figure 3-7b shows, each amino acid contains a central carbon atom covalently bonded to four other atoms or functional groups. A single hydrogen atom, highlighted in blue in the illustration, bonds at one site. A carboxyl group, —COOH, highlighted in green, bonds at a second site. An amino group, —NH2, highlighted in yel- low, bonds at a third site. A side chain called the R group, high- lighted in red, bonds at the fourth site. The main difference among the different amino acids is in their R groups. The R group can be complex or it can be simple, such as the CH3 group shown in the amino acid alanine in Figure 3-7b. The differences among the amino acid R groups gives different proteins very different shapes. The different shapes allow pro- teins to carry out many different activities in living things. Amino acids are commonly shown in a simplified way such as balls, as shown in Figure 3-7c. (a) Many structures, such as hair and horns are made of proteins. (b) Proteins are made up of amino acids. Amino acids differ only in the type of R group (shown in red) they carry. Polar R groups can dissolve in water, but nonpolar R groups cannot. (c) Amino acids have complex structures, so, in this and other textbooks, they are often simplified into balls. FIGURE 3-7 (b) Alanine (an amino acid) (c) Simplified version of amino acid CH3 H N OH C C H O H (a) Copyright © by Holt, Rinehart and Winston. All rights reserved. BIOCHEMISTRY 57 H H N C C OH H O H CH3 H2O Glycine Alanine H N OH C C H O H H H N C C H O H CH3 N OH C C H O H (a) (b) (a) The peptide bond (shaded blue) that binds amino acids together to form a polypeptide results from a condensation reaction that produces water. (b) Poly- peptides are commonly shown as a string of balls in this textbook and elsewhere. Each ball represents an amino acid. FIGURE 3-8 Substrate Products Enzyme 1 2 3 In the induced fit model of enzyme action, the enzyme can attach only to a substrate (reactant) with a specific shape. The enzyme then changes and reduces the activation energy of the reaction so reactants can become products. The enzyme is unchanged and is available to be used again. 3 2 1 FIGURE 3-9 Dipeptides and Polypeptides Figure 3-8a shows how two amino acids bond to form a dipeptide (die-PEP-TIED). In this condensation reaction, the two amino acids form a covalent bond, called a peptide bond (shaded in blue in Figure 3-8a) and release a water molecule. Amino acids often form very long chains called polypeptides (PAHL-i-PEP-TIEDZ). Proteins are composed of one or more polypep- tides. Some proteins are very large molecules, containing hun- dreds of amino acids. Often, these long proteins are bent and folded upon themselves as a result of interactions—such as hydrogen bonding—between individual amino acids. Protein shape can also be influenced by conditions such as temperature and the type of solvent in which a protein is dissolved. For exam- ple, cooking an egg changes the shape of proteins in the egg white. The firm, opaque result is very different from the initial clear, runny material. Enzymes Enzymes—RNA or protein molecules that act as biological catalysts—are essential for the functioning of any cell. Many enzymes are proteins. Figure 3-9 shows an induced fit model of enzyme action. Enzyme reactions depend on a physical fit between the enzyme molecule and its specific substrate, the reactant being catalyzed. Notice that the enzyme has folds, or an active site, with a shape that allows the substrate to fit into the active site. An enzyme acts only on a specific substrate because only that substrate fits into its active site. The linkage of the enzyme and substrate causes a slight change in the enzyme’s shape. The change in the enzyme’s shape weakens some chemical bonds in the substrate, which is one way that enzymes reduce activation energy, the energy needed to start the reaction. After the reaction, the enzyme releases the products. Like any catalyst, the enzyme itself is unchanged, so it can be used many times. An enzyme may not work if its environment is changed. For example, change in temperature or pH can cause a change in the shape of the enzyme or the substrate. If such a change happens, the reaction that the enzyme would have catalyzed cannot occur.Cell Size Cells differ not only in their shape but also in their size. A few types of cells are large enough to be seen by the unaided human eye. For example, the nerve cells that extend from a giraffe’s spinal cord to its foot can be 2 m (about 6 1/2 ft) long. A human egg cell is about the size of the period at the end of this sentence. Most cells, how- ever, are only 10 to 50 μm in diameter, or about 1/500 the size of the period at the end of this sentence. The size of a cell is limited by the relationship of the cell’s outer surface area to its volume, or its surface area–to-volume ratio. As a cell grows, its volume increases much faster than its surface area does, as shown in Figure 4-5. This trend is important because the materials needed by a cell (such as nutrients and oxygen) and the wastes produced by a cell (such as carbon dioxide) must pass into and out of the cell through its surface. If a cell were to become very large, the volume would increase much more than the surface area. Therefore, the surface area would not allow materials to enter or leave the cell quickly enough to meet the cell’s needs. As a result, most cells are microscopic in size. Comparing Surface Cells Materials microscope, prepared slides of plant (dicot) stem and ani- mal (human) skin, pencil, paper Procedure Examine slides by using medium magnification (100). Observe and draw the sur- face cells of the plant stem and the animal skin. Analysis How do the surface cells of each organism differ from the cells beneath the surface cells? What is the function of the surface cells? Explain how surface cells are suited to their function based on their shape. Quick Lab Small cells can exchange substances more readily than large cells because small objects have a higher surface area–to-volume ratio. FIGURE 4-5 mb06se_csfs02.qxd 5/18/07 10:54 AM Page 73 74 CHAPTER 4 BASIC PARTS OF A CELL Despite the diversity among cells, three basic features are common to all cell types. All cells have an outer boundary, an interior sub- stance, and a control region. Plasma Membrane The cell’s outer boundary, called the plasma membrane (or the cell membrane), covers a cell’s surface and acts as a barrier between the inside and the outside of a cell. All materials enter or exit through the plasma membrane. The surface of a plasma mem- brane is shown in Figure 4-6a. Cytoplasm The region of the cell that is within the plasma membrane and that includes the fluid, the cytoskeleton, and all of the organelles except the nucleus is called the cytoplasm. The part of the cytoplasm that includes molecules and small particles, such as ribosomes, but not membrane-bound organelles is the cytosol. About 20 percent of the cytosol is made up of protein. Control Center Cells carry coded information in the form of DNA for regulating their functions and reproducing themselves. The DNA in some types of cells floats freely inside the cell. Other cells have a mem- brane-bound organelle that contains a cell’s DNA. This membrane- bound structure is called the nucleus. Most of the functions of a eukaryotic cell are controlled by the cell’s nucleus. The nucleus is often the most prominent structure within a eukaryotic cell. It maintains its shape with the help of a protein skeleton called the nuclear matrix. The nucleus of a typical animal cell is shown in Figure 4-6b. Most animal cells have a cell membrane, a nucleus, and a variety of other organelles embedded in a watery substance. The surface of the cell membrane can be seen in (a). The organelles inside the cell are labeled in the diagram (b). FIGURE 4-6 (a) (b) Mitochondrion Microfilaments Lysosome Golgi apparatus Smooth ER Ribosomes Cell membrane Microtubules Rough ER Nuclear pore Nuclear envelope Nucleolus Nucleus Copyright © by Holt, Rinehart and Winston. All rights reserved. Cell wall Ribosome Cell membrane Peptidoglycan Pili Flagellum DNA CELL STRUCTURE AND FUNCTION 75 A prokaryotic cell lacks a membrane- bound nucleus and membrane-bound organelles. Most prokaryotic cells are much smaller than eukaryotic cells are. FIGURE 4-7 A white blood cell (eukaryotic) changes shape as it attacks purple- stained bacterial cells that are much smaller (prokaryotic). FIGURE 4-8 TWO BASIC TYPES OF CELLS Fossil evidence suggests that the earliest cells on Earth were simple cells similar to some present-day bacteria. As cells evolved, they differentiated into two major types: prokaryotes and eukaryotes. Prokaryotes Prokaryotes (proh-KAR-ee-OHTS) are organisms that lack a membrane- bound nucleus and membrane-bound organelles. Although prokaryotic cells lack a nucleus, their genetic information—in the form of DNA—is often concentrated in a part of the cell called the nucleoid. Figure 4-7 shows a typical prokaryotic cell. Prokaryotes are divided into two domains: Bacteria and Archaea (ahr-KEE-uh). The domain Bacteria includes organisms that are similar to the first cellular life-forms. The domain Archaea includes organisms that are thought to be more closely related to eukaryotic cells found in all other kingdoms of life. Eukaryotes Organisms made up of one or more cells that have a nucleus and membrane-bound organelles are called eukaryotes (yoo-KAR-ee-OHTS). Eukaryotic cells also have a variety of subcellular structures called organelles, well-defined, intracellular bodies that perform specific functions for the cell. Many organelles are surrounded by a mem- brane. The organelles carry out cellular processes just as a person’s pancreas, heart, and other organs carry out a person’s life processes. Eukaryotic cells are generally much larger than prokary- otic cells, as seen in Figure 4-8, which shows a white blood cell (eukaryote) destroying tiny bacterial cells (prokaryotes).