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Higher 2.6 Biology
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by having sterile conditionsÂ
by growing them in a fermentor
by mutagenesis or recombinant DNA technology
exposure to UV light and other forms of radiation or mutagenic chemicals
putting it in sterile conditions
growing it with other microorganisms
Cells of different organisms and even cells within the same organism are very diverse in terms of shape, size, and internal organization. One theme that occurs again and again throughout biology is that form follows function. In other words, a cellâs function influences its physical features. Cell Shape The diversity in cell shapes reflects the different functions of cells. Compare the cell shapes shown in Figure 4-4. The long extensions that reach out in various directions from the nerve cell shown in Figure 4-4a allow the cell to send and receive nerve impulses. The flat, platelike shape of skin cells in Figure 4-4b suits their function of covering and protecting the surface of the body. As shown below, a cellâs shape can be simple or complex depending on the function of the cell. Each cell has a shape that has evolved to allow the cell to perform its function effectively. SECTION 2 OBJECTIVES â Explain the relationship between cell shape and cell function. â Identify the factor that limits cell size. â Describe the three basic parts of a cell. â Compare prokaryotic cells and eukaryotic cells. â Analyze the relationship among cells, tissues, organs, organ systems, and organisms. VOCABULARY plasma membrane cytoplasm cytosol nucleus prokaryote eukaryote organelle tissue organ organ system Cells have various shapes. (a) Nerve cells have long extensions. (b) Skin cells are flat and platelike. (c) Egg cells are spherical. (d) Some bacteria are rod shaped. (e) Some plant cells are rectangular. FIGURE 4-4 (a) Nerve cell (b) Skin cells (c) Egg cell (d) Bacterial cells (e) Plant cells Copyright © by Holt, Rinehart and Winston. All rights reserved. 1. All cubes have volume and surface area. The total surface area is equal to the sum of the areas of each of the six sides (area = length X width). 2. If you split the first cube into eight smaller cubes, you get 48 sides. The volume remains constant, but the total surface area doubles. 3. If you split each of the eight cubes into eight smaller cubes, you have 64 cubes that together contain the same volume as the first cube. The total surface area, however, has doubled again. CELL STRUCTURE AND FUNCTION 73 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 giraffeâs 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 ÎŒm 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 cellâs outer surface area to its volume, or its surface areaâto-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 cellâs 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 areaâto-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 cellâs outer boundary, called the plasma membrane (or the cell membrane), covers a cellâs 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 cellâs DNA. This membrane- bound structure is called the nucleus. Most of the functions of a eukaryotic cell are controlled by the cellâs 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
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 DesirĂ©e Nieuwenhuis | NatĂ lia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. Dif- ferential role of adipose tissues in obesity and related metabolic and vas- cular complications. 2016;2016:1-15, 1216783. 6. Zwick RK, Guerrero-Juarez CF, Horsley V, Plikus MV. Anatomical, physiological, and functional diversity of adipose tissue. Cell Metab. 2018;27(1):68-83. 7. Gulyaeva O, Dempersmier J, Sul HS. Genetic and epigenetic control of adipose development. Biochimica et Biophysica Acta (BBA)â Molecular and Cell Biology of Lipids. 2019;1864:3-12. 8. Khan M, Joseph F. Adipose tissue and adipokines: the association with and application of adipokines in obesity. Forensic Sci. 2014;2014: 711-724, 328592. 9. Alotaibi MF. Physiology of puberty in boys and girls and pathological disorders affecting its onset. J Adolesc. 2019;71:63-71. 10. Cousminer DL, Stergiakouli E, Berry DJ, et al. Genome-wide associa- tion study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty. Hum Mol Genet. 2014;23(16):4452-4464. 11. Ahmed ML, Ong KK, Dunger DB. Childhood obesity and the timing of puberty. Trends in endocrinology and metabolism: TEM. 2009;20(5): 237-242. 12. Biro FM, Pajak A, Wolff MS, et al. Age of menarche in a longitudinal US cohort. J Pediatr Adolesc Gynecol. 2018;31(4):339-345. 13. Currie C, Ahluwalia N, Godeau E, Nic Gabhainn S, Due P, Currie DB. Is obesity at individual and national level associated with lower age at menarche? Evidence from 34 countries in the Health Behaviour in School-aged Children Study. The Journal of adolescent health: official publication of the Society for Adolescent Medicine. 2012;50(6): 621-626. 14. De Leonibus C, Marcovecchio ML, Chiavaroli V, de Giorgis T, Chiarelli F, Mohn A. Timing of puberty and physical growth in obese children: a longitudinal study in boys and girls. Pediatr Obes. 2014; 9(4):292-299. 15. Flom JD, Cohn BA, Tehranifar P, et al. Earlier age at menarche in girls with rapid early life growth: cohort and within sibling analyses. Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, WidĂ©n E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999â2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, Schönbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. Böttner A, Jr K, MĂŒller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, Iñiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. Corrigendum to: Increased high molecular weight adiponectin, but decreased total adiponectin and kisspeptin, in central precocious puberty compared with aged-matched prepubertal girls. Reprod Fertil Dev. 2017;29:2506-2517. 64. Das UN. Is obesity an inflammatory condition? Nutrition. 2001; 17(11-12):953-966. 65. Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Hum Reprod Update. 2014; 20(2):153-174. 66. Singh A, Choubey M, Bora P, Krishna A. Adiponectin and chemerin: contrary adipokines in regulating reproduction and metabolic disor- ders. Reproductive sciences (Thousand Oaks, Calif). 2018;25:1462- 1473. 67. Tsatsanis C, Dermitzaki E, Avgoustinaki P, Malliaraki N, Mytaras V, Margioris AN. The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis. Hormones (Athens). 2015; 14:549-562. 68. Kang MJ, Oh YJ, Shim YS, Baek JW, Yang S. Hwang IT. The usefulness of circulating levels of leptin, kisspeptin, and neurokinin B in obese girls with precocious puberty. 2018;34:627-630. 69. Lee J, Song J, Hootman JM, et al. Obesity and other modifiable fac- tors for physical inactivity measured by accelerometer in adults with knee osteoarthritis: data from the osteoarthritis initiative (OAI). Arthritis Care Res (Hoboken). 2012;53-61. 70. Bramswig J, Dubbers A. Disorders of pubertal development. Deutsches Arzteblatt international. 2009;106:295-303. quiz 04 71. Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertil- ity. Cell Mol Life Sci. 2013;70(5):841-862. 72. Riumallo J, Durnin JV. Changes in body composition in adolescent boys. Eur J Clin Nutr. 1988;42(2):107-112. 73. Siervogel RM, Demerath EW, Schubert C, et al. Puberty and body composition. Horm Res. 2003;60(Suppl 1):36-45. 74. Zhang J. Gong M. Andrologia: Review of the role of leptin in the regu- lation of male reproductive function; 2018. 75. Kauffman AS, Gottsch ML, Roa J, et al. Sexual differentiation of Kiss1 gene expression in the brain of the rat. Endocrinology. 2007;148(4): 1774-1783. 76. Zeydabadi Nejad S, Ramezani Tehrani F, Zadeh-Vakili A. The role of kisspeptin in female reproduction. Int J Endocrinol Metab. 2017;15:1- 11, e44337. 77. Sorensen K, Aksglaede L, Petersen JH, Juul A. Recent changes in pubertal timing in healthy Danish boys: associations with body mass index. J Clin Endocrinol Metab. 2010;95(1):263-270. 78. Juul A, Magnusdottir S, Scheike T, Prytz S, Skakkebaek NE. Age at voice break in Danish boys: effects of pre-pubertal body mass index and secular trend. Int J Androl. 2007;30(6):537-542. 79. Lee JM, Wasserman R, Kaciroti N, et al. Timing of puberty in overweight versus obese boys. Pediatrics. 2016;137(2):137-146, e20150164. 80. He F, Guan P, Liu Q, Crabtree D, Peng L, Wang H. The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. Secondary sexual characteristics in boys: data from the Pediatric Research in Office Settings Network. Pediatrics. 2012;130(5):e1058-e1068. 86. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452. 87. Akin I, Tolg R, Hochadel M, et al. No evidence of âobesity paradoxâ after treatment with drug-eluting stents in a routine clinical practice: results from the prospective multicenter German DES.DE (German Drug-Eluting Stent) Registry. JACC Cardiovasc Interv. 2012;5(2): 162-169. 88. Marcovecchio ML, Chiarelli F. Obesity and growth during childhood and puberty. World Rev Nutr Diet. 2013;106:135-141. How to cite this article: Nieuwenhuis D, Pujol-Gualdo N, Arnoldussen IAC, Kiliaan AJ. Adipokines: A gear shift in puberty. Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are gover
Can you make a multiple choice of test questions regarding this information given which is Curriculum from Different Points of View There are many definitions of curriculum. Because of this, the concept of curriculum is sometimes characterized as fragmentary, elusive and confusing. However, the numerous definitions indicate dynamism that connotes diverse interpretations of what curriculum is all about. The definitions are influenced by models of thought, pedagogies, political as well as cultural experiences. Let us study some of these definitions. 1. Traditional Points of View of Curriculum In early years of the 20th century, the traditional concepts held of the âcurriculum is that it is a body of subjects or subject matter prepaid by the teachers for the studentâs to learnâ. It was synonymous to the âcourse of studyâ and âsyllabusâ Robert M. Hutchins views curriculum as âpermanent studiesâ where the rules of grammar, reading, rhetoric and logic and mathematics for basic education are emphasized. Basic education should emphasize the 3 Rs and college education should be grounded on liberal education. On the other, Arthur Bestor as an essentialist, believes that the mission of the school should be intellectual training, hence curriculum should focus on the fundamental intellectual disciplines of grammar, literature and writing. It should also include mathematics, science, history and foreign language. The definition leads us to the view of Joseph Schwab that discipline is the sole source of curriculum. Thus in our education system, curriculum is divided into chunks of knowledge we call subject areas in basic education such as English, Mathematics, Science, Social Studies and others. In college, discipline may include humanities, sciences, language and many more. To Phoenix, curriculum should consist entirely of knowledge which comes from various disciplines. Academic discipline became the view of what curriculum is after the cold war and the race to space. Joseph Schwab, a leading curriculum theorist coined the term discipline as a ruling doctrine for curriculum development. Curriculum should consist only of knowledge which comes from disciplines which is the sole source. Thus curriculum can be viewed as a field of study. It is made up of its foundations (philosophical, historical, psychological and social foundations); domains of knowledge as well as its research theories and principles. Curriculum is taken as scholarly and theoretical. It is concerned with broad historical, philosophical and social issues and academics. Most of the traditional ideas view curriculum as written documents or a plan of action in accomplishing goals. 2. Progressive Points of View of Curriculum On the other hand, to a progressivist, a listing of school subjects, syllabi, course of study, and a list of courses or specific discipline do not make a curriculum. These can only be called curriculum if the written materials are actualized by the learner. Broadly speaking, curriculum is defined as the total learning experiences of the individual. This definition is anchored on John Deweyâs definition of experience and education. He believed that reflective thinking is a means that unifies curricular elements. Thought is not derived from action but tested by application. Caswell and Campbell viewed curriculum as âall experiences children have under the guidance of teachersâ. This definition is shared by Smith, Stanley and Shores when they defined âcurriculum as a sequence of potential experiences set up in the schools for the purpose of disciplining children and youth in group ways of thinking and actingâ. Marsh and Willis on the other hand view curriculum as all the âexperiences in the classroom which are planned and enacted by the teacher, and also learned by the studentsâ. Points of View on Curriculum Development From the various definitions and concepts presented, it is clear that curriculum is a dynamic process. Development connotes changes which are systematic. A change for the better means any alteration, modification or improvement of existing condition. To produce positive changes, development should be purposeful, planned and progressive. This is how curriculum evolves. Let us look at the two models of curriculum development and concepts of Ralph Tyler and Hilda Taba. Ralph Tyler Model: Four Basic Principles. This is also popularly known as Tylerâs Rationale. He posited four fundamental questions or principles in examining any curriculum in schools. These four fundamental principles are as follows: 1. What educational purposes should the school seek to attain? 2. What educational experiences can be provided that are likely to attain these purposes? 3. How can these educational experiences be effectively organized? 4. How can we determine whether these purposes are being attained or not? In summary, Tylerâs Model show that in curriculum development, the following considerations should be made: (1) Purpose of the school, (2) Educational experiences related to the purposes, (3) Organization of the experiences, and (4) Evaluation of the experiences. On the other hand, Hilda Taba improved on Tylerâs Rationale by making a linear model. She believed that teachers who teach or implement the curriculum should participate in developing it. Her advocacy was commonly called the grassroots approach. She presented seven major steps to her model where teachers could have a major input. These steps are as follows: 1. Diagnosis of learnerâs needs and expectations of the larger society. 2. Formulation of learning objectives. 3. Selection of learning content. 4. Organization of learning content. 5. Selection of learning experiences. 6. Organization of learning activities. 7. Determination of what to evaluate and the means of doing it. Thus as you look into curriculum models, the three interacting processes in curriculum development are planning, implementing and evaluating. Types of Curriculum Operating in Schools From the various concepts given, Allan Glatthorn(2000) describes seven types of curriculum operating in the schools. These are (1) Recommended curriculum- proposed by scholars and professional organizations. (2) Written Curriculum- appears in school, district, division or country documents. (3) Taught Curriculum- what teacherâs implement or deliver in the classrooms and schools. (4) Supported Curriculum- resources-textbooks, computers, audio- visual materials which support and help in the implementation of the curriculum. (5) Assessed Curriculum- that which is tested and evaluated. (6) Learned Curriculum- which the students actually learn and what is measured and (7) Hidden Curriculum- the unintended curriculum. 1. Recommended Curriculum- Most of the school curricula are recommended. The curriculum may come from a national agency like the Department of Education, Commission on Higher Education (CHED), Department of Science and Technology (DOST) or any professional organization who has stake in education. For example the Philippine Association for Teacher Education (PAFTE) or the Biology Teacher Association (BIOTA) may recommend a curriculum to be implemented in the elementary or secondary education. 2. Written Curriculum- This includes documents, course of study or syllabi handed down to the schools, districts, division, departments or colleges for implementation. Most of the written curricula are made by curriculum experts with participation of teachers. These were pilot-tested or tried out in sample schools or population. Example of this is the Basic Education Curriculum (BEC). Another example is the written lesson plan of each classroom teacher made up of objectives and planned activities of the teacher. 3. Taught Curriculum- The different planned activities which are put into action in the classroom compose the taught curriculum. These are varied activities that are implemented in order to arrive at the objectives or purposes of the written curriculum. These are used by the learners with the guidance of teachers. Taught curriculum varies according to the learning styles of students and the teaching styles of teachers. 4. Supported Curriculum- In order to have a successful teaching, other than the teacher, there must be materials which should support or help in the implementation of a written curriculum. These refer to the support curriculum that includes material resources such as textbooks, computers, audio-visual materials, laboratory equipment, playgrounds, zoos and other facilities. Support curriculum should enable each learner to achieve real and lifelong learning. 5. Assessed Curriculum- This refers to a tested or evaluated curriculum. At the duration and end of the teaching episodes, series of evaluations are being done by the teachers to determine the extent of teaching or to tell if the students are progressing. This refers to the assessed curriculum. Assessment tools like pencil-and-paper tests, authentic instruments like portfolio are being utilized. 6. Learned Curriculum- This refers the learning outcomes achieved by the students. Learning outcomes are indicated by the results of the tests and changes in behavior which can either be cognitive, affective or psychomotor. 7. Hidden Curriculum- This is the unintended curriculum which is not deliberately planned but may modify behavior or influenced learning outcomes. There are lots of hidden curricula that transpire in the schools. Peer influence, school environment, physical condition, teacher-learner interaction, mood of the teachers and many other factors made up the hidden curriculum.
Lide 1: Introduction to Bioreactor A bioreactor is a vessel used for growing microorganisms, plant or animal cells Provides controlled conditions for biological reactions Maintains optimum pH, temperature, oxygen, and nutrients Widely used in fermentation, enzyme, vaccine, and antibiotic production Ensures sterile and aseptic environment Scale ranges from laboratory to industrial production Slide 2: Basic Design Requirements of a Bioreactor Must be constructed with non-toxic, corrosion-resistant materials Should allow effective mixing and mass transfer Provision for sterilization (in situ sterilization) Must maintain uniform temperature and pH Easy sampling without contamination Should support scalability and automation Slide 3: Materials Used in Bioreactor Construction Stainless steel (SS-316) for industrial bioreactors Glass for laboratory-scale bioreactors Plastic (polycarbonate) for disposable bioreactors Materials must withstand heat and pressure Should be smooth to prevent microbial attachment Resistant to chemicals and cleaning agents Slide 4: Main Parts of a Bioreactor Vessel: holds the culture medium and microorganisms Agitator (impeller): provides mixing Sparger: supplies sterile air Baffles: prevent vortex formation Sensors: monitor pH, temperature, dissolved oxygen Ports: used for inoculation, sampling, and feeding Slide 5: Agitation System Ensures uniform mixing of nutrients and cells Improves oxygen transfer rate Common impellers: Rushton turbine, marine propeller Speed controlled by motor Prevents settling of cells Affects shear stress on cells Slide 6: Aeration System Supplies oxygen for aerobic fermentation Air introduced through sparger Types of spargers: ring, nozzle, sintered Maintains dissolved oxygen concentration Air is filtered for sterility Essential for high cell density cultures Slide 7: Temperature and pH Control Temperature controlled by heating/cooling jackets pH maintained using acid or alkali addition Sensors continuously monitor parameters Automated control systems used Ensures optimal microbial growth Prevents enzyme denaturation Slide 8: Foam Control System Foam formed due to protein and agitation Excess foam reduces oxygen transfer Mechanical foam breakers used Chemical antifoam agents added Foam sensor detects foam formation Maintains efficient fermentation Slide 9: Types of Bioreactors â Based on Mode of Operation Batch bioreactor Fed-batch bioreactor Continuous bioreactor Choice depends on product type Widely used in industrial fermentation Controls productivity and yield Slide 10: Batch Bioreactor All nutrients added at the beginning No addition or removal during process Simple and easy to operate Low risk of contamination Used for antibiotics and enzymes Limited control over nutrient depletion Slide 11: Fed-Batch Bioreactor Nutrients added during fermentation Prevents substrate inhibition High product yield Widely used in industrial fermentation Allows better control of growth rate Used in insulin and enzyme production Slide 12: Continuous Bioreactor Fresh medium continuously added Culture removed at same rate Maintains steady-state conditions High productivity Risk of contamination is high Used in wastewater treatment and SCP production Slide 13: Types of Bioreactors â Based on Design Stirred tank bioreactor Airlift bioreactor Bubble column bioreactor Packed bed bioreactor Fluidized bed bioreactor Photobioreactor Slide 14: Stirred Tank Bioreactor (STR) Most commonly used bioreactor Mechanical agitation using impellers Suitable for aerobic fermentation Excellent mixing and oxygen transfer Used for bacteria and fungi Easy scale-up Slide 15: Airlift Bioreactor Mixing achieved by air circulation No mechanical agitator Low shear stress Energy efficient Suitable for shear-sensitive cells Used in wastewater treatment Slide 16: Bubble Column Bioreactor Air bubbles provide mixing Simple design and low cost No moving parts Limited mixing efficiency Used for microbial fermentation Suitable for large-scale operations Slide 17: Packed Bed Bioreactor Contains immobilized cells or enzymes Substrate flows through packed matrix High cell density Used in continuous processes Limited oxygen transfer Used in enzyme and wastewater treatment Slide 18: Fluidized Bed Bioreactor Immobilized particles kept in suspension Better mass transfer than packed bed Reduced clogging Suitable for continuous operation Used in biotransformations Higher operational complexity Slide 19: Photobioreactor Designed for photosynthetic organisms Provides light source Used for algae and cyanobacteria Controls light, COâ, and temperature Used in biofuel and pigment production Can be tubular or flat-plate design Slide 20: Applications of Bioreactors Production of antibiotics and vaccines Enzyme and organic acid production Single cell protein production Wastewater treatment Biofertilizer and biopesticide production Biopharmaceutical manufacturing
20. Ang unang yugto sa pagbuo ng Community-Based Disaster Risk Reduction Management (CBDRRM) Plan ay tinatawag na ________. A. pagtugon sa sakuna B. paghahanda sa pagtugon C. pagsasaayos at pagbangon D. pagtataya ng panganib at paghahanda ANSWER: D 21. Ang gawaing ito ay isinasagawa upang maging handa ang komunidad at maiwasan ang malawakang pinsala nito sa pamamagitan ng aktibong pakikibahagi ng mamamayan. Ito ay nakapaloob sa _______. A. Philippine Disaster Risk Management B. Philippine Disaster Risk Reduction Management Council C. Community Preparedness and Risk Management Approach D. Community-Based Disaster Risk Reduction Management Approach ANSWER: D 22. Bahagi ng rehabilitasyon at pagbawi mula sa kalamidad ang mga hakbang at gawain na nakatuon sa pagsasaayos ng mga nasirang pasilidad at estruktura. Ano ang pangunahing gampanin ng yugtong ito? A. Mabigyan ng sapat na proteksiyon ang mga nasalanta ng kalamidad. B. Manumbalik sa dating kaayusan at normal na pamumuhay ang mga nasalantang komunidad. C. Makapagbigay ng mga inaasahang serbisyong panlipunan at paglilingkod sa pamahalaan. D. Maipagkaloob sa mga nasalantang komunidad ang mga pangunahing pangangailangan at gamot. ANSWER: B 23. Alin sa sumusunod na mga sitwasyon ang nagpapakita ng Top-Down Approach sa pagbuo ng Disaster Risk Reduction and Management (DRRM) Plan? A. Pinamunuan ni Kerwin, isang lider ng Non-Government Organization (NGO) ang pagtukoy sa mga kalamidad na maaaring maranasan sa kanilang komunidad. B. Ipinatawag ni Kapitan Capin ang kaniyang mga kagawad upang bumuo ng plano kung paano magiging ligtas ang kaniyang nasasakupan mula sa panganib ng paparating na bagyo. C. Hinikayat ni Albert ang kaniyang mga kapitbahay na maglinis ng estero upang maiwasan ang pagbara nito na maaaring magdulot ng malalim at matagalang pagbaha sa darating na tag-ulan. D. Nakipag-usap si Kelly sa mga may-ari ng malalaking negosyo sa kanilang komunidad upang makalikom ng pondo sa pagbili ng mga first aid kit at iba pang proyekto bilang paghahanda sa ibaât ibang kalamidad. ANSWER: B 24. Bakit mahalaga ang pagkakaroon ng community engagement o kolaborasyon sa pamayanan at iba pang katuwang na sektor? A. Makatutulong ito upang makalikom ng mas maraming pondo. B. Magiging makabuluhan ang plano kung ang gagawa nito ay ang mamamayan. C. Malaki ang posibilidad na maging matagumpay ang proyekto kapag pinagplanuhan. D. Mas magiging komprehensibo at matagumpay ang plano kung binubuo ito ng ibaât ibang sektor. ANSWER: D 25. Sa pagbuo ng CBDRRM Plan, ano ang PINAKAMABISA mong nararapat gawin bilang mamamayan ng isang lugar upang maging handa sa pagdating ng ibaât ibang panganib at kalamidad? A. Maging aktibong kabahagi sa pagbubuo ng plano para sa buong pamayanan. B. Makibahagi sa gawaing panrehabilitasyon at tulungan ang mga naapektuhan. C. Magsagawa ng personal plan para matugunan ang pangangailangan ng lipunan. D. Magkaroon ng planong pampinansiyal upang matustusan ang pangangailangan ng mga tao. ANSWER: A 26. Ang pinuno ng mga bansang kasapi ng organisasyon ay nagpupulong-pulong upang magtulungan para sa kapakanan ng kanilang pangangailangan. Anong anyo ng globalisasyon ang tinutukoy nito? A. ekonomiko B. kultural C. politikal D. teknolohikal ANSWER: C 27. Alin sa sumusunod ang buhay na manipestasyon ng globalisasyon? A. ekonomiko B. OFWs C. sosyo-kultural D. teknolohikal ANSWER: B 28. Ang brain drain ay tumutukoy sa mga propesyonal na manggagawa, samantalang ang brawn drain ay tumutukoy sa ___________. A. construction workers B. domestic workers C. overseas workers D. skilled workers ANSWER: A 29. Alin sa sumusunod ang negatibong epekto ng paglitaw ng maraming multinational companies at transnational companies? A. pagkakaloob ng hanapbuhay B. pagbaba ng presyo ng produkto C. pagdami ng produkto at serbisyo D. pagkalugi ng multinational companies at transnational companies ANSWER: D 30. âAng globalisasyon ay laganap na noon pa man at naging mas malawak sa kasalukuyang panahon.â Ang mahihinuha natin sa pahayag na ito ay _______. A. ugnayan ng mga bansa sa daigdig na walang pagitan o hadlang B. suliraning panlipunan na pumipigil sa kaunlaran ng mga bansa sa daigdig C. bagong anyo ng malayang kalakalan, pagpapalitan ng produkto, impormasyon at tao, dahil sa pag-unlad ng teknolohiya sa komunikasyon at transportasyon D. isyung panlipunan na tumatalakay sa pamahalaan, ekonomiya, relihiyon, teknolohiya, kapaligiran, komunikasyon at kultura ng mga bansa sa daigdig ANSWER: C 31. Alin sa dalawang pahayag ang nagsasaad ng PINAKAANGKOP na konsepto ng globalisasyon? I. Ang globalisasyon ay proseso ng mabilisang pagdaloy o paggalaw ng tao, bagay, impormasyon at produkto sa ibaât ibang direksiyon na nararanasan sa ibaât ibang panig ng daigdig. II. Ang globalisasyon ay may ibaât ibang pagkakakilanlan tulad ng ekonomiko, teknolohikal, sosyo-kultural at politikal. A. Mali ang nilalaman ng una at ikalawang pahayag. B. Tama ang nilalaman ng una at ikalawang pahayag. C. Tama ang nilalaman ng una at mali ang ikalawang pahayag. D. Mali ang nilalaman ng una at tama ang ikalawang pahayag. ANSWER: B 32. Alin sa sumusunod na mga pahayag ang nagsasaad ng dahilan sa pag-usbong ng globalisasyon? A. pagbuti ng mga lokal na kompanya sa presyo at kalidad ng serbisyo at produkto upang maging kompetitibo laban sa mga banyagang kompanya B. pagpapalitan ng impormasyon at teknolohiya at paggalaw ng mga tao dulot ng migrasyon C. pagbaba ng sahod ng mga manggagawa at pagdami ng mga taong walang trabaho dahil nalulugi ang maliliit na negosyo D. paglaganap ng biological weapons dulot ng mabilis na pagkalat ng impormasyon sa ibaât ibang panig ng mundo at pagdami ng pamilihan ng materyales na ginagamit dito ANSWER: B 33. Alin sa mga sektor ng manggagawa ang madalas nakararanas ng pang-aabuso at hindi pantay na oportunidad sa pagtratrabaho? A. agrikultura B. industriya C. pamahalaan D. serbisyo ANSWER: A 34. Ano ang tawag sa anyo ng subcontracting kung saan ang mga subcontractor ay may sapat na puhunan para maisagawa ang trabaho ng mga manggagawang ipinasok nila? A. iskemang subcontractor B. job mismatch C. job contracting D. labor-only contracting ANSWER: C 35. Bakit hindi maitaas ang pasahod, maipagkaloob ang kasiguraduhan sa trabaho, at madagdagan ang benepisyo ng mga manggagawa sa bansa? Ito ay dahil_____ A. sa sistema ng kontraktuwalisasyon. B. puro regular na ang mga manggagawa. C. mataas na ang pasahod sa ating manggagawa. D. marami ang benepisyong natatanggap ng ating manggagawa. ANSWER: A 36. Bilang tugon sa suliraning nararanasan ng mga manggagawa, mayroon silang karapatang hindi dapat malabag upang masabi na sila ay may disente at marangal na hanapbuhay. Alin sa sumusunod ang HINDI kabilang sa mga karapatan ng manggagawa? A. Karapatan sa pantay na suweldo para sa parehong trabaho. B. Karapatang sumali sa marahas at mapanganib na uri ng unyon. C. Karapatang maging ligtas at malayo sa panganib ang kalagayan ng pagtatrabaho. D. Karapatan na makatanggap ng sapat at karapat-dapat na suweldo para sa makataong pamumuhay. ANSWER: B 37. Halos mapudpod na ang sapatos ni Justin sa paghahanap ng trabaho ngunit hindi pa rin siya natatanggap. Maraming job fairs na rin ang kaniyang pinuntahan ngunit bigo siyang makakuha ng trabaho. Bakit kaya ito nangyayari kay Justin? A. Kulang pa ang kaniyang lakas ng loob. B. Kulang siya sa aspekto ng personal relations kaya hindi siya nagugustuhan. C. Hindi kaaya-aya ang kaniyang pisikal na kaanyuan kaya hindi siya natatanggap sa trabaho. D. Biktima si Justin ng job mismatch kung saan hindi tugma ang kaniyang kakayahan at kasanayan na hinahanap ng mga kompanya. ANSWER: D 38. Ayon sa tala ng Department of Labor and Employment (DOLE), maraming job fairs noong 2010 ngunit kakaunti lamang ang mga natanggap na kalipikadong aplikante mula sa maraming bilang ng mga nag-apply. Alin ang HINDI angkop na dahilan nito? A. Ang mga aplikante ay hindi interesado sa mga trabaho sa bansa. B. Kapansin-pansin ang patuloy na paglaki ng bilang ng job skills mismatch ng mga aplikante sa bansa. C. May patuloy na mismatch sa kasanayan at kakayahan mula sa tinapos na kurso at sa hinihinging kalipikasyon ng mga employer. D. Maraming kurso sa higher education institutions sa bansa ang hindi na tumutugon sa pangangailangan ng mga pribadong kompanya na nagtatakda ng mga pamantayan sa pagpili ng mga manggagawa. ANSWER: A 39. Alin ang angkop na salita na tumutukoy sa sitwasyon kung saan inaako na ng lalaki ang mga gawain sa tahanan dulot ng migrasyon? A. helper B. house boy C. house father D. house husband ANSWER: D 40. Ang sumusunod ay mga ahensiya ng pamahalaan na nangangalaga sa kapakanan ng migrante MALIBAN sa __________________. A. Commission of Filipino Overseas B. Philippine Overseas Labor Offices C. Department of Labor and Employment D. Department of Science and Technology ANSWER: D 41. Isang epekto ng migrasyon ay ang pagtanggap o pagpapadala ng mga lakas-paggawa sa ibang bansa. Alin sa sumusunod ang HINDI nagpapakita ng magandang benepisyo ng brain gain? A. Malaki ang posibilidad ng promotion ng manggagawa. B. Gastusin ng kompanya ang pagpapadala ng manggagawa sa ibang bansa. C. Maaaring magtrabaho sa ibang bansa ang empleadong ipinadala upang matuto. D. Magiging asset ang migranteng manggagawa sa nagpapadala at tumatanggap na bansa kahit saan man sa mundo. ANSWER: B 42. Matagal na naghanapbuhay si Ginoong Pascual sa Australia, kaya sa kaniyang pag-uwi sa pamilya ay hindi siya pinansin ng kaniyang mga anak at nagtago ang mga ito sa kuwarto. Ano ang iyong mahihinuha rito? A. Malaki ang takot ng mga anak sa kanilang ama. B. Walang pasalubong si Ginoong Pascual sa mga anak. C. Hindi kilala si Ginoong Pascual ng kaniyang mga anak. D. Nagkakahiyaan ang mag-aama sa kanilang pagkikita. ANSWER: C 43. Paano nakaaapekto ang pangingibang-bansa sa estado ng ekonomiya ng bansa? A. Madaragdagan ang populasyon ng bansa. B. Mapananatiling matatag ang palitan ng piso at dolyar. C. Mahihirapan ang mga Pilipino na makisama sa mga dayuhan. D. Mas maraming papasok sa bansa na mga imported na produkto. ANSWER: B 44. Marami sa mga OFW na nasa Middle East ang napag-alamang nakararanas ng mga pang-aabuso mula sa kanilang mga amo tulad sa Saudi Arabia. Kung ikaw ang ambassador ng Pilipinas sa Saudi, alin ang pinakamabisa mong gagawin upang matulungan at maprotektahan sila? A. Pababayaan sila hanggang matapos ang kanilang kontrata. B. Maglulunsad ng rally sa embahada ng Saudi Arabia sa Pilipinas. C. Hihingi ng tulong pinansiyal at pauuwiin ang mga manggagawa sa Saudi. D. Maglilikom ng mga ebidensiya ng mga pang-aabuso at isusuplong ang mga amo sa kinauukulan. ANSWER: D 45. Alin sa sumusunod ang konseptong tumutukoy sa slavery? A. pang-aalipin B. sitwasyong payapa C. sapilitang pagtatrabaho D. pagpupuslit ng mga tao ANSWER: A 46. Kung ikaw ay opisyal ng pamahalaan na nangangalaga sa kapakanan ng mga OFW, alin sa sumusunod ang dapat mong gawin sa mga kaso ng pang-aabuso sa mga Pilipino? A. Pauuwiin ang lahat ng OFW at bibigyan na lamang ng trabaho sa Pilipinas. B. Pababayaan na lamang ang mga OFW dahil isolated cases lang naman ang mga ito. C. Ipauubaya na lamang ang mga gagawing aksiyon sa pamahalaan ng bansa kung saan nagtatrabaho ang mga OFW. D. Magtatatag ng mga mekanismo upang ma-monitor ang kalagayan ng mga OFW at gagawa ng kaukulang hakbang kung may pang-aabuso. ANSWER: D 47. Bilang isang mag-aaral sa kasalukuyan, alin sa sumusunod ang maaari mong magawa upang masigurong makaaangkop ka sa pangangailangan ng ating bansa na umunlad sa kabila ng globalisasyon? A. Magpalipas ng panahon at umasa na lamang sa pamilya. B. Tumigil sa pag-aaral at magtrabaho na upang kumita ng pera. C. Magsumikap sa pag-aaral upang makatapos at magkatrabaho. D. Maging layunin ang makapagtrabaho sa ibang bansa upang yumaman. ANSWER: C 48. Alin sa sumusunod na mga pangungusap ang tumutukoy sa konsepto ng fair trade? A. Itinatakda ng mga bansa ang pamantayan ukol sa mga kakayahan ng mga manggagawa. B. Ang mayayamang bansa ay nagbibigay ng tulong sa pinakamahihirap na tao sa mundo lalo na sa Aprika at Asya. C. Sinisiguro ng mga bansa ang patas o pantay na kalakalan gaya ng pagbabantay sa tamang presyo ng mga produkto. D. Ang pamahalaan ay nakikialam sa kalakalang panlabas na may layong protektahan ang mga lokal na namumuhunan. ANSWER: C 49. Marami sa mga pamilya ng OFWs ay nakararanas ng pangungulila sa kanilang kaanak na humahantong sa pagkawasak nito. Paano kaya sila matutulungan? A. Makisimpatiya sa kanila. B. Bigyan sila ng sulat isa-isa. C. Bigyan sila ng load pantawag sa kanilang kaanak. D. Magtayo ng isang samahan ng mga pamilya ng OFW upang gumabay sa kanila. ANSWER: D 50. Sa Pilipinas ay marami ang nangangarap na mangibang-bansa dulot ng kahirapan sa buhay. Nangangamba naman ang mga ekonomista dahil naaapektuhan ng brain drain at brawn drain ang ekonomiya. Bilang ekonomista, ano ang maaari mong gawin upang masolusyunan ang isyung ito? A. Pigilan ang mga nais mangibang-bansa. B. Hayaang umalis ang mga nais na magtrabaho sa ibang bansa. C. Bigyan ng suportang pinansiyal ang mamamayan na walang trabaho. D. Gumawa ng isang development plan na tutugon sa mga isyu ng migrasyon. ANSWER: D
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 giraffeâs 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 ÎŒm 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 cellâs outer surface area to its volume, or its surface areaâto-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 cellâs 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 areaâto-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 cellâs outer boundary, called the plasma membrane (or the cell membrane), covers a cellâs 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 cellâs DNA. This membrane- bound structure is called the nucleus. Most of the functions of a eukaryotic cell are controlled by the cellâs 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 informationâin the form of DNAâis 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 personâs pancreas, heart, and other organs carry out a personâs 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).
LESSON 4. Cellular Respiration âą Define cellular respiration âą Identify the stages of clan respiration You have just learned how the energy from the sun is captured, processed, and stored in the form of glucose. Cellular respiration, another important life process, is the means by which cells release the stored energy in glucose to make adenosine triphosphate (ATP). The primary goal of this life process is to convert stored energy into usable form, such as ATP, for the cells to carry out their functions. Cellular respiration involves several chemical reactions. The reactions can be summed up in the following equation: C6 H12 O6 + 602 -----ï 6 COâ +6HâO + ATP Glucose oxygen carbon dioxide water energy Aerobic respiration reactions, or cellular respiration that takes place in the presence of oxygen, can be grouped into three stages glycolysis, Krebs cycle, and electron transport chain (ETC). Stage 1: Glycolysis Glycolysis is the process that breaks down one molecule of 6-C glucose into 3-C pyruvates or pyruvic acids. It also releases four molecules of ATP. This process occurs in the cytoplasm of the cell. The following is the step-by-step process of glycolysis. Take note that several enzymes are involved in this process. 1. The first step of glycolysis requires energy. It can only proceed when the two ATP molecules donate energy to the glucose by transferring a phosphate group with the help of an enzyme, producing glucose 6-phosphate 2. Then, a specific enzyme promotes the rearrangement of the atoms, producing the fructose 6-phosphate. 3. The action of the enzyme in step 2 promotes the transfer of a phosphate group from another ATP molecule, forming fructose 1,6-bisphosphate. 4. The resulting fructose 1,6-bisphosphate molecules, with the help of another enzyme, splits into two molecules, each with three carbon backbones. These two sugars are dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. 5. Another important enzyme then rapidly interconverts the molecules of dihydro-xyacetone phosphate and glyceraldehyde 3-phosphate. This produces two molecules of glyceraldehyde 3-phosphate or 3-phosphoglyceraldehyde (PGAL) 6. The succeeding step involves another enzyme-mediated action. The hydrogen (H) from PGAL is transferred to the oxidizing agent, nicotinamide adenine dinucleotide (NAD), which forms NADH. A phosphate (P) is also added from the cytosol of the cell to oxidize the two molecules of PGAL, forming two 1.3-bisphosphoglycerate. 7. A phosphate (P) from 1,3-biphosphoglycerate is transferred to ADP to form ATP. This happens for each of the two 1,3-bisphosphoglycerate. resulting to a yield of two ATP and two 3-phosphoglycerate molecules. 8. A phosphate is transferred from 3-phosphoglycerate molecules from the third carbon to the second carbon, forming 2-phosphoglycerate molecules A hydrogen atom and a hydroxyl ((OH) group is released, which then combines to form water (H2O). The removal of H2O from 2-phosphoglycerate results in the formation of 2- phosphoglycerate molecules. 9. A hydrogen atom and a hydroxyl ((OH) group is released, which then combines to form water (H2O). The removal of H2O from 2-phosphoglycerate results in the formation of two phosphoenolpyruvic acid (PEP) 10. Phosphate (P) from PEP is transferred to ADP (and forms ATP) and the final product, pyruvic acid. This reaction yields two molecules of pyruvic acid and two ATP molecules In summary, a single glucose molecule that undergoes the process of glycolysis produces two molecules of pyruvic acid, four molecules of ATP, two molecules of NADEL and two molecules of H.O. However, only two molecules of ATP are counted as net products since two molecules of ATP are spent throughout the process. Stage II: Krebs Cycle The Krebs cycle, named after its proponent Sir Hans Adolf Krebs, is a cyclical series of enzyme-controlled reactions. This stage of cellular respiration occurs in the matrix of the mitochondria. It is sometimes. called the citric acid cycle (CAC) since it produces citric acid. Citric acid contains three carboxyl (COOH) groups; hence, it is also called the tricarboxylic acid cycle (TCA). This requires the pyruvic acids produced during glycolysis. The main function of this cycle is to produce high-energy-yielding molecules, namely, NADH and flavin adenine dinucleotide (FADH) that will later on be used in the electron transport chain reaction. Figure 6-7. Summary of glycolysis and corresponding products in each reaction presented (See Appendix F on page 285 for an enlarged and complete version of the image.) An initial process is needed for the Krebs cycle to begin. As a pyruvate molecule from glycolysis enters the mitochondrion, it undergoes an important preliminary ate to form acetyl-CoA reaction. Coenzyme-A (COA) combines with pyruvate help of an enzymatic complex. This conversion also produces CO, and NADH. The Krebs cycle is summarized as follows. Take note that several enzymes are involved in this process. 1. The Krebs cycle technically begins when the acetyl-CoA combines with oxaloacetic acid (OAA), a 4-C molecule, to produce citric acid, a 6-C molecule. 2. With the aid of an enzyme, the citric acid now goes through a series of reactions that releases energy. Water molecule is removed from the citric acid and is returned in a different location. The-OH group is repositioned, forming the molecule isocitrate. 3. Isocitrate is then oxidized, forming the a-ketoglutarate, a 5-C molecule. The byproducts of this reaction are NADH and CO, 4 The a-ketoglutarate loses its CO, and a coenzyme-A is added in its place. The decarboxylation occurs with the help of NAD, which then becomes NADH. The resulting molecule is called succinyl-CoA. 5. Succinyl-CoA is converted into succinate. Also in this reaction, a molecule of guanosine triphosphate (GTP) is synthesized. The GTP molecule has similar structure and energy properties to that of ATP and is used by cells the same way. The free phosphate group attacks the succinyl-CoA molecule, which detaches the COA. Then, phosphate is attached to GDP to come up with GTP, similar to the process that occur in ATP synthesis (from ADP to ATP). 6. Two hydrogens are removed from succinate, A molecule of flavin adenine dinucleotide (FAD), a coenzyme similar to NAD, is reduced to FADH, as it takes the hydrogens from the succinate. This reaction produces the fumarate. 7. Fumarate is then converted into malate as the addition of a water molecule is catalyzed. The final reaction is the regeneration of oxaloacetate. The resulting byproduct of this regeneration is NADH Recall that two pyruvate molecules were produced during glycolysis, causing the Krebs cycle to turn twice. Each tuts produces three molecules of NADH, single ATH one FADIH, and the by-product CO, which is exhaled. Stage III: Electron Transport Chain The electron transport chain (ETC) is a series of photon pumps on the inner membrane of the mitochondrion. Electron transport is the last stage of the cellular respiration. In this stage, the energy from NADH and FADH, from the Krebs cycle is transferred to ADP to produce ATP. This process is generally known as oxidative phosphorylation. This energy coupling mechanism in the cell was revealed by the work of Peter stored energy in the form of proton (1) gradient to phosphorylate (add phosphate) ADP and produce ATP. The pumping of hydrogen sons across the inner membrane creates higher concentration ions in the inner membrane than on the outside of the membrane. This chemiosmotic gradient causes the ions to flow back across the membrane where the concentration of ions is lower. ATP synthase lined in the matrix serve as a channel protein, helping the ions to move across the membrane. The chemiosmotic gradient powers the phosphorylation of ADP to ATP, which also occurs in the ATP synthase. After passing through the ETC, the oxygen, being the final hydrogen acceptor, combines with two electrons and two protons, forming a water molecule. Water is a by-product of cellular respiration and is excreted. MINI TEST 6-3 1. Which energy-releasing pathway yields the most ATF in each glucose molecule? 2. Briefly describe the two stages of aerobic respiration that follow glycolysis: (a) Krebs cycle (b) Electron transport chain Anaerobic Respiration Most cells carry out arrobic respiration when oxygen is present. Aerobic respiration is an efficient process that yields a lot of ATP. However, many organisms thrive in mud, marshes, animal gut, canned goods, sewage treatment pond, and deep oceans where oxygen is scarce. Organisms that can live without oxygen are called anaerobes. Cellular respiration that proceeds without the presence of oxygen is called anaerobic respiration. In the event that the oxygen supply becomes low, aerobic cells also perform fermentation and lactic acid fermentation anaerobic pathways. There are two common anaerobic pathways in these cells, alcoholic fermentation and lactic acid fermentation. In alcoholic fermentation, ethyl alcohol and carbon dioxide are produced by some cells using the pyruvate from glycolysis. Each pyruvate molecule is rearranged into acetaldehyde and carbon dioxide, which is eventually released. NADII gives up electrons to acetaldehyde to form ethanol Fermentation is widely used in the industry. Yeast, a fungus used in making bread. can undergo anaerobic respiration. Bakers aux sugar, flour, water, and yeast to form the bread dough. The dough rises due to the carbon dioxide and alcohol released by the yeast cells trapped in air bubbles. Beer and wine manufacturers, we yeast to ferment the sugars in wheat and grape juice, forming alcoholic beverages such as beer and wine. In some cells, glycolysis produces two pyruvates, two NADH molecules, and two ATP molecules. Pyruvate itself becomes the final acceptor of the electrons from the NADH that produces the final product: lactate. Oftentimes, this product is called lactic acid. Human skeletal muscles can carry out fermentation when the blood cannot supply the cells with adequate oxygen during strenuous activities. When lactic acid builds up in the muscles, fatigue, burning sensation, and cramps result. Lactic acid will continue to build up until there is adequate supply of oxygen. Lactic acid is then converted back into pyruvate in the liver. Muscles also restore normal functions. Have you ever wondered why milk or cream turns sour after some time? Bacterial cells that undergo fermentation are responsible in producing lactate that turns the milk sour. These bacteria are used in manufacturing yogurt and sour milk products. Fermentation pathways do not breakdown and utilize the glucose completely. ATP is no longer produced beyond the process of glycolysis. Thus, energy produced is just enough for some single-celled organisms, or the energy can only be used by multicellular organisms for a short period.
1. SA node sends an impulse causing the atria to contract 2. Blood moves from the right atrium into the right ventricle past the tricuspid valve 3. Blood moves from the left atrium into the left ventricle past the mitral or bicuspid valve 4. Impulse pauses at AV node to allow for maximum blood to be squeezed into the ventricles 5. Impulse travels to the AV bundle (or bundle of His) and down the bundle branches 6. Impulse travels out Purkinje fibers causing the apex to contract 7. The apex contraction increases the blood pressure in the ventricles causing the Mitral and Tricuspid (AV) valves to close. 8. Atria repolarize and begin to fill 9. Purkinje fibers cause the ventricle walls and papillary muscles to depolarize (contract) 10. Papillary muscles hold the AV valves shut (keep them from prolapsing) through the chordae tendineae connection 11. The aortic and pulmonary semilunar valves open when the pressure is higher in the ventricles than in the major arteries 12. Blood moves from right ventricle to pulmonary trunk/arteries past the pulmonary semilunar valve 13. Blood moves from left ventricle to aorta past the aortic semilunar valve 14. Blood pathway is arteries to arterioles, to capillaries (or capillary bed), to venules, veins and vena cava back to the right atrium 15. The ventricles start to repolarize (relax) which decreases the pressure in the ventricles 16. When the pressure is lower in the ventricles than in the major arteries, blood moves back toward heart shutting semilunar valves 17. When the aortic valve closes, the openings to the coronary arteries are exposed 18. Back pressure in the aorta pushes blood out the left and right coronary arteries supplying the heart with oxygenated blood 19. The AV valves open and blood moves from the atria into the ventricles when the ventricular pressure falls below atrial pressure. 20. The process starts again when the SA node fires causing the atria to contract.