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Best Practice & Research. Clinical... Jan 2022Puberty marks the end of childhood and is a period when individuals undergo physiological and psychological changes to achieve sexual maturation and fertility. The onset... (Review)
Review
Puberty marks the end of childhood and is a period when individuals undergo physiological and psychological changes to achieve sexual maturation and fertility. The onset of puberty is first detected as an increase in pulsatile secretion of gonadotropin-releasing hormone (GnRH). Pubertal onset is regulated by genetic, nutritional, environmental, and socio-economic factors. Disturbances affecting pubertal timing result in adverse health conditions later in life. Human genetic studies show that around 50-80% of the variation in pubertal onset is genetically determined. The genetic control of pubertal timing has been a field of active investigation in attempt to better understand the neuroendocrine control of this relevant period of life. Large populational studies and patient cohort-based studies have provided insights into the genetic regulation of pubertal onset. In this review, we discuss these discoveries and discuss potential mechanisms for how implicated genes may affect pubertal timing.
Topics: Gonadotropin-Releasing Hormone; Humans; Puberty; Puberty, Delayed; Sexual Maturation
PubMed: 35183440
DOI: 10.1016/j.beem.2022.101618 -
Current Opinion in Endocrinology,... Feb 2018The current review summarizes recent epidemiologic data demonstrating the effects of endocrine disrupting compounds (EDCs) on the timing of puberty and highlights the... (Review)
Review
PURPOSE OF REVIEW
The current review summarizes recent epidemiologic data demonstrating the effects of endocrine disrupting compounds (EDCs) on the timing of puberty and highlights the complexity of understanding the interplay of environmental and genetic factors on pubertal timing.
RECENT FINDINGS
In girls, there have been mixed results, with some exposures being associated with earlier timing of puberty, and some with later puberty. In boys, prepubertal exposures to nondioxin-like polychlorinated biphenyls accelerate puberty, whereas levels of insecticides, dioxin-like compounds, organochlorine pesticides, and lead delay puberty.
SUMMARY
The effects of EDCs on pubertal timing are sexually dimorphic, compound specific, and varies according to the window of exposure. These studies confirm that low-level exposures to a mix of environmental compounds may mask the effects of individual compounds and complicate our ability to translate data from animal studies to human health and to fully understand the clinical implications of environmental epidemiology studies.
Topics: Animals; Endocrine Disruptors; Environmental Exposure; Female; Humans; Male; Pesticides; Puberty; Sexual Maturation; Time Factors
PubMed: 29135489
DOI: 10.1097/MED.0000000000000377 -
Ciencia & Saude Coletiva Sep 2022This study aimed to investigate the relationship between sexual maturation and anthropometric and blood pressure indicators in teenagers. This was a population-based...
This study aimed to investigate the relationship between sexual maturation and anthropometric and blood pressure indicators in teenagers. This was a population-based cross-sectional study, conducted with 345 teenagers, aged 10 to 19 years, between 2018 and 2020. In this study, data referent to sociodemographic and anthropometric variables, blood pressure, and sexual maturation were collected. The data analysis was performed by applying the Principle Component Analysis (PCA), which generated three components and then tested the correlation between sexual maturation and the generated components. Most of the teenagers were female (53%), normotensive (66.1%), and with a normal weight (73%). A positive correlation was found between breast development and component 1 and component 2, as well as a negative correlation between the breasts and component 3. In the boys, the development of genitals and pubic hair was positively correlated with component 2 and inversely correlated with component 3. It could therefore be concluded that there is a relationship between sexual maturation and the anthropometric and blood pressure indicators, which proved to be representative variables for cardiovascular risk in teenagers, even if not in their entirety.
Topics: Adolescent; Anthropometry; Blood Pressure; Cross-Sectional Studies; Female; Humans; Male; Sexual Maturation
PubMed: 36000648
DOI: 10.1590/1413-81232022279.04622022 -
Metabolism: Clinical and Experimental Sep 2018The understanding of adipose tissue role has evolved from that of a depot energy storage organ to a dynamic endocrine organ. While genetics, sexual phenotype and sex... (Review)
Review
The understanding of adipose tissue role has evolved from that of a depot energy storage organ to a dynamic endocrine organ. While genetics, sexual phenotype and sex steroids can impact the mass and distribution of adipose tissue, there is a counter-influence of white adipocytes on reproduction. This primarily occurs via the secretion of adipokines, the most studied of which- leptin and adiponectin- are highlighted in this article. Leptin, the "satiety hormone" primarily acts on the hypothalamus via pro-opiomelanocortin (POMC), neuropeptide Y (NPY), and agouti-related peptide (AgRP) neurons to translate acute changes in nutrition and energy expenditure, as well as chronic adipose accumulation into changes in appetite and potentially mediate insulin resistance via shared pathway and notably impacting reproductive health via influence on GnRH secreting neurons. Meanwhile, adiponectin is notable for its action in mediating insulin sensitivity, with receptors found at every level of the reproductive axis. Both have been examined in the context of physiologic and pathologic reproductive conditions. Leptin has been shown to influence puberty, pregnancy, hypothalamic amenorrhea, and lipodystrophy, and with a potential therapeutic role for both metabolic and reproductive health. Adiponectin mediates the relative state of insulin resistance in pregnancy, and has been implicated in conditions such as polycystic ovary syndrome and reproductive malignancies. There are numerous other adipokines, including resistin, visfatin, chemerin and retinol binding protein-4, which may also play roles in reproductive health and disease states. The continued examination of these and other adipokines in both normal reproduction and reproductive pathologies represents an important avenue for continued study. Here, we seek to provide a broad, yet comprehensive overview of many facets of these relationships and highlight areas of consideration for clinicians and future study.
Topics: Adipose Tissue; Animals; Female; Humans; Leptin; Obesity; Pregnancy; Reproduction; Reproductive Health; Sexual Maturation
PubMed: 29155136
DOI: 10.1016/j.metabol.2017.11.006 -
Seminars in Reproductive Medicine Jul 2019Puberty is a fundamental developmental event in the lifespan of any individual, when sexual and somatic maturation is completed, and reproductive capacity is achieved.... (Review)
Review
Puberty is a fundamental developmental event in the lifespan of any individual, when sexual and somatic maturation is completed, and reproductive capacity is achieved. While the tempo of puberty is under strong genetic determination, it is also modulated by a wide array of internal and environmental cues, including, prominently, nutritional and metabolic signals. In the last decade, our understanding of the neurohormonal basis of normal puberty and its perturbations has enlarged considerably. This is illustrated by the elucidation of the essential roles of kisspeptins, encoded by the Kiss1 gene, in the hypothalamic circuits controlling puberty. Moreover, other neuropeptide pathways, convergent with kisspeptin signaling, have been pointed out as important coregulators of pubertal timing. These include the cotransmitters of Kiss1 neurons in the arcuate nucleus (ARC), neurokinin B, and dynorphin, as well as melanocortins, produced by ARC neurons expressing proopiomelanocortin, which are endowed with key roles also in the control of metabolic homeostasis. This neuropeptide setup seemingly participates, in a coordinated manner, in transmitting the regulatory actions of metabolic cues on pubertal maturation. In this function, cellular metabolic sensors, such as the AMP-activated protein kinase, and the fuel-sensing deacetylase, SIRT1, have also been shown recently to contribute to the metabolic regulation of puberty. Altogether, elucidation of the physiological roles of these signals and regulatory circuits will help uncover the intimacies of the brain control of puberty, and its alterations in conditions of metabolic stress, ranging from subnutrition to obesity.
Topics: Animals; Humans; Hypothalamus; Kisspeptins; Neurokinin B; Neurons; Neuropeptides; Puberty; Reproduction; Sexual Maturation; Signal Transduction
PubMed: 31972860
DOI: 10.1055/s-0039-3400967 -
Frontiers in Endocrinology 2023
Topics: Sexual Maturation; Humans; Puberty
PubMed: 37560304
DOI: 10.3389/fendo.2023.1258656 -
Molecular Reproduction and Development Feb 2017Teleost fish exhibit remarkably diverse and plastic patterns of sexual development. One of the most fascinating modes of plasticity is functional sex change, which is... (Review)
Review
Teleost fish exhibit remarkably diverse and plastic patterns of sexual development. One of the most fascinating modes of plasticity is functional sex change, which is widespread in marine fish including species of commercial importance; however, the regulatory mechanisms remain elusive. In this review, we explore such sexual plasticity in fish, using the bluehead wrasse (Thalassoma bifasciatum) as the primary model. Synthesizing current knowledge, we propose that cortisol and key neurochemicals modulate gonadotropin releasing hormone and luteinizing hormone signaling to promote socially controlled sex change in protogynous fish. Future large-scale genomic analyses and systematic comparisons among species, combined with manipulation studies, will likely uncover the common and unique pathways governing this astonishing transformation. Revealing the molecular and neuroendocrine mechanisms underlying sex change in fish will greatly enhance our understanding of vertebrate sex determination and differentiation as well as phenotypic plasticity in response to environmental influences. Mol. Reprod. Dev. 84: 171-194, 2017. © 2016 Wiley Periodicals, Inc.
Topics: Animals; Female; Fishes; Gonadotropin-Releasing Hormone; Luteinizing Hormone; Male; Sex Determination Processes; Sexual Maturation; Signal Transduction
PubMed: 27543780
DOI: 10.1002/mrd.22691 -
Molecular Ecology Sep 2021Sexual maturation timing is a life-history trait central to the balance between mortality and reproduction. Maturation may be triggered when an underlying compound...
Sexual maturation timing is a life-history trait central to the balance between mortality and reproduction. Maturation may be triggered when an underlying compound trait, called liability, exceeds a threshold. In many different species and especially fishes, this liability is approximated by growth and body condition. However, environmental vs. genetic contributions either directly or via growth and body condition to maturation timing remain unclear. Uncertainty exists also because the maturation process can reverse this causality and itself affect growth and body condition. In addition, disentangling the contributions of polygenic and major loci can be important. In many fishes, males mature before females, enabling the study of associations between male maturation and maturation-unbiased female liability traits. Using 40 Atlantic salmon families, longitudinal common-garden experimentation, and quantitative genetic analyses, we disentangled environmental from polygenic and major locus (vgll3) effects on male maturation, and sex-specific growth and condition. We detected polygenic heritabilities for maturation, growth, and body condition, and vgll3 effects on maturation and body condition but not on growth. Longitudinal patterns for sex-specific phenotypic liability, and for genetic variances and correlations between sexes suggested that early growth and condition indeed positively affected maturation initiation. However, towards spawning time, causality appeared reversed for males whereby maturation affected growth negatively and condition positively via both the environmental and genetic effects. Altogether, the results indicate that growth and condition are useful traits to study liability for maturation initiation, but only until maturation alters their expression, and that vgll3 contributes to maturation initiation via condition.
Topics: Animals; Female; Humans; Life History Traits; Male; Phenotype; Reproduction; Salmo salar; Sexual Maturation; Transcription Factors
PubMed: 34228841
DOI: 10.1111/mec.16062 -
Pediatrics in Review Jul 2016
Review
Topics: Adolescent; Child; Female; Humans; Male; Puberty; Sexual Maturation
PubMed: 27368360
DOI: 10.1542/pir.2015-0065 -
Pediatrics Apr 2024
Topics: Male; Female; Humans; Sexual Maturation
PubMed: 38545672
DOI: 10.1542/peds.2023-064452