-
Animal : An International Journal of... May 2023This article reviews the scientific literature on puberty with a focus on ruminants and draws inference, where appropriate, from recent findings in transgenic mouse... (Review)
Review
This article reviews the scientific literature on puberty with a focus on ruminants and draws inference, where appropriate, from recent findings in transgenic mouse models and human pathology. Early genetic determinants of puberty have been discovered in humans suffering from hypogonadotropic hypogonadism or central precocious puberty. Transgenic mouse models selected on the basis of the causative defective genes helped in discovering the cellular and molecular mechanisms involved. Most of the genes found are involved in the development of neuroendocrine networks during embryo development and early postnatal life. Notwithstanding that the development of neuroendocrine networks takes place early in puberty, a delay or acceleration in the development of Gonadotropin Releasing Hormone (GnRH) neurons has an impact on puberty onset inducing a delay or an advance, respectively. Among the genes discovered in humans and laboratory models, only a few of them displayed polymorphisms associated with advanced sexual maturity, but also marbling, growth traits and callipygian conformation. This could be related to the fact that rather than puberty onset, most research monitored sexual maturity. Sexual maturity occurs after puberty onset and involves factors regulating the maturation of gonads and in the expression of sexual behaviour. The association with growth and metabolic traits is not surprising since nutrition is the major environmental factor that will act on late genetic determinants of puberty onset. However, a recent hypothesis emerged suggesting that it is the postnatal activation of the GnRH neuronal network that induces the acceleration of growth and weight gain. Hence, nutritional factors need the activation of GnRH neurons first before acting on late genetic determinants. Moreover, nutritional factors can also affect the epigenetic landscape of parental gamete's genome with the consequence of specific methylation of genes involved in GnRH neuron development in the embryo. Season is another important regulator of puberty onset in seasonal small ruminants and appears to involve the same mechanisms that are involved in seasonal transition in adults. The social environment is also an underestimated factor affecting puberty onset in domestic ruminants, most research studies focused on olfactory cues, but the genetic basis has not heretofore been adequately tackled by the scientific community. Additionally, there is some evidence to suggest transgenerational effects exist, in that nutritional and social cues to which parents were exposed, could affect the epigenetic landscape of parental gametes resulting in the epigenetic regulation of early genetic determinants of puberty onset in their offspring.
Topics: Mice; Humans; Animals; Sexual Maturation; Epigenesis, Genetic; Puberty; Gonadotropin-Releasing Hormone; Ruminants; Mice, Transgenic
PubMed: 37567653
DOI: 10.1016/j.animal.2023.100812 -
International Journal of Public Health 2023To investigate the associations of obesity with growth and puberty in children. From November 2017 to December 2019, height, weight, and Tanner stages of 26,879...
To investigate the associations of obesity with growth and puberty in children. From November 2017 to December 2019, height, weight, and Tanner stages of 26,879 children aged 3-18 years in Fuzhou, China were assessed. The obese group was significantly taller than the non-obese group after age 4 years for both genders, yet there was no significant difference in height between obese and non-obese group after 15.5 years old for boys and 12.5 years old for girls. The inflection points of significant growth deceleration in obese and non-obese groups were 14.4 and 14.6 years old for boys, and 11.8 and 12.8 years old for girls, respectively. The proportions of testicular development in boys with obesity and non-obesity were 7.96% and 5.08% at 8.5-8.9 years old, respectively, while the proportions of breast development in girls were 17.19% and 3.22% at age 7.5-7.9 years old, respectively. Children with obesity were taller in early childhood, earlier onset of puberty and earlier cessation of growth than children with non-obesity of the same age. However, there was sex dimorphism on the effect of obesity on the incidence of precocious puberty.
Topics: Humans; Child; Child, Preschool; Female; Male; Adolescent; Cross-Sectional Studies; Obesity; Puberty; Puberty, Precocious; China
PubMed: 37255545
DOI: 10.3389/ijph.2023.1605433 -
Nutrients May 2024The onset of puberty, which is under the control of the hypothalamic-pituitary-gonadal (HPG) axis, is influenced by various factors, including obesity, which has been... (Review)
Review
The onset of puberty, which is under the control of the hypothalamic-pituitary-gonadal (HPG) axis, is influenced by various factors, including obesity, which has been associated with the earlier onset of puberty. Obesity-induced hypothalamic inflammation may cause premature activation of gonadotropin-releasing hormone (GnRH) neurons, resulting in the development of precocious or early puberty. Mechanisms involving phoenixin action and hypothalamic microglial cells are implicated. Furthermore, obesity induces structural and cellular brain alterations, disrupting metabolic regulation. Imaging studies reveal neuroinflammatory changes in obese individuals, impacting pubertal timing. Magnetic resonance spectroscopy enables the assessment of the brain's neurochemical composition by measuring key metabolites, highlighting potential pathways involved in neurological changes associated with obesity. In this article, we present evidence indicating a potential association among obesity, hypothalamic inflammation, and precocious puberty.
Topics: Humans; Pediatric Obesity; Hypothalamus; Child; Puberty, Precocious; Puberty; Inflammation; Female; Gonadotropin-Releasing Hormone; Male; Hypothalamo-Hypophyseal System
PubMed: 38892653
DOI: 10.3390/nu16111720 -
Tidsskrift For Den Norske Laegeforening... May 2021
Topics: Humans; Puberty
PubMed: 33950643
DOI: 10.4045/tidsskr.21.0210 -
Blood Feb 2021
Topics: Anemia, Sickle Cell; Antisickling Agents; Humans; Hydroxyurea; Male; Puberty; Spermatozoa
PubMed: 33570610
DOI: 10.1182/blood.2020008803 -
The Journal of Adolescent Health :... Jan 2020
Topics: Adolescent; Female; Gender Equity; Gender Identity; Humans; Male; Puberty
PubMed: 31866032
DOI: 10.1016/j.jadohealth.2019.10.012 -
Developmental Cognitive Neuroscience Apr 2023Pubertal development is a potential trigger for increases in risk-taking behaviours during adolescence. Here, we sought to investigate the relationship between puberty...
Pubertal development is a potential trigger for increases in risk-taking behaviours during adolescence. Here, we sought to investigate the relationship between puberty and neural activation during risky decision-making in males using functional magnetic resonance imaging (fMRI). Forty-seven males aged 12.5-14.5 years completed an fMRI risk-taking task (BART) and reported their tendencies for risky decision-making using a self-report questionnaire. Puberty was assessed through self-reported pubertal status and salivary testosterone levels. Testosterone concentration, but not physical pubertal status, was positively correlated with self-reported risk-taking behaviour, while neither was correlated with BART performance. Across the whole sample, participants had greater activation of the bilateral nucleus accumbens and right caudate on trials when they made a successful risky decision compared to trials when they made a safe choice or when their risky decision was unsuccessful. There was a negative correlation between pubertal stage and brain activation during unsuccessful risky decision-making trials compared within unsuccessful control trials. Males at a lower stage of pubertal development showed increased activation in the left insula, right cingulate cortex, dorsomedial prefrontal cortex (dmPFC), right putamen and right orbitofrontal cortex (OFC) relative to more pubertally mature males during trials when they chose to take a risk and the balloon popped compared to when they watched the computer make an unsuccessful risky decision. Less pubertally mature males also showed greater activation in brain regions including the dmPFC, right temporal and frontal cortices, right OFC, right hippocampus and occipital cortex in unsuccessful risky trials compared to successful risky trials. These results suggest a puberty-related shift in neural activation within key brain regions when processing outcomes of risky decisions, which may reduce their sensitivity to negative feedback, and in turn contribute to increases in adolescent risk-taking behaviours.
Topics: Humans; Male; Adolescent; Decision Making; Risk-Taking; Brain; Puberty; Brain Mapping; Magnetic Resonance Imaging; Testosterone
PubMed: 36965437
DOI: 10.1016/j.dcn.2023.101230 -
International Journal of Environmental... Apr 2022In the COVID-19 pandemic, there was an increase in consultations for precocious puberty. We aim to analyze differences in female puberty before and during the COVID-19...
In the COVID-19 pandemic, there was an increase in consultations for precocious puberty. We aim to analyze differences in female puberty before and during the COVID-19 pandemic. A cross-sectional analytical study was designed at the Pediatric Endocrinology Clinic of the University Hospital of the Federal University of Maranhão in São Luis, Brazil. We included 55 girls with precocious puberty, 22 who started puberty during the pandemic and 33 who started puberty before the pandemic. Clinical, anthropometric, laboratory and imaging variables were compared between groups. Statistics were performed to determine if there was a statistical difference between the groups. Girls with puberty during the pandemic had higher Z-scores for weight (1.08 ± 1.29 versus 0.69 ± 0.83; = 0.04), lower ovarian volume (1.88 ± 0.95 versus 3.15 ± 2.31; = 0.01), and smaller differences between thelarche noticed by the parents and the diagnosis (6.63 ± 5.21 versus 12.15 ± 9.96; = 0.02). The association between precocious puberty during the pandemic with higher Z-scores for weight, lower ovarian volume, and a reduction in the time between the perception of pubertal findings by parents and the diagnosis suggests the influence of the pandemic on the normal time of puberty.
Topics: COVID-19; Child; Cross-Sectional Studies; Female; Humans; Male; Pandemics; Puberty; Puberty, Precocious
PubMed: 35457600
DOI: 10.3390/ijerph19084733 -
Biology Letters Sep 2023There is considerably greater variation in metabolic rates between men than between women, in terms of basal, activity and total (daily) energy expenditure (EE). One...
There is considerably greater variation in metabolic rates between men than between women, in terms of basal, activity and total (daily) energy expenditure (EE). One possible explanation is that EE is associated with male sexual characteristics (which are known to vary more than other traits) such as musculature and athletic capacity. Such traits might be predicted to be most prominent during periods of adolescence and young adulthood, when sexual behaviour develops and peaks. We tested this hypothesis on a large dataset by comparing the amount of male variation and female variation in total EE, activity EE and basal EE, at different life stages, along with several morphological traits: height, fat free mass and fat mass. Total EE, and to some degree also activity EE, exhibit considerable greater male variation (GMV) in young adults, and then a decreasing GMV in progressively older individuals. Arguably, basal EE, and also morphometrics, do not exhibit this pattern. These findings suggest that single male sexual characteristics may not exhibit peak GMV in young adulthood, however total and perhaps also activity EE, associated with many morphological and physiological traits combined, do exhibit GMV most prominently during the reproductive life stages.
Topics: Adolescent; Young Adult; Female; Humans; Male; Adult; Puberty; Sexual Behavior; Reproduction; Energy Metabolism; Phenotype
PubMed: 37727077
DOI: 10.1098/rsbl.2023.0152 -
Brain Research Bulletin Aug 2023Illness is often predicated long before the manifestation of its symptoms. Exposure to stressful experiences particularly during critical periods of development, such as... (Review)
Review
Illness is often predicated long before the manifestation of its symptoms. Exposure to stressful experiences particularly during critical periods of development, such as puberty and adolescence, can induce various physical and mental illnesses. Puberty is a critical period of maturation for neuroendocrine systems, such as the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal (HPA) axes. Exposure to adverse experiences during puberty can impede normal brain reorganizing and remodelling and result in enduring consequences on brain functioning and behaviour. Stress responsivity differs between the sexes during the pubertal period. This sex difference is partly due to differences in circulating sex hormones between males and females, impacting stress and immune responses differently. The effects of stress during puberty on physical and mental health remains under-examined. The purpose of this review is to summarize the most recent findings pertaining to age and sex differences in HPA axis, HPG axis, and immune system development, and describe how disruption in the functioning of these systems can propagate disease. Lastly, we delve into the notable neuroimmune contributions, sex differences, and the mediating role of the gut microbiome on stress and health outcomes. Understanding the enduring consequences of adverse experiences during puberty on physical and mental health will allow a greater proficiency in treating and preventing stress-related diseases early in development.
Topics: Adolescent; Humans; Male; Female; Hypothalamo-Hypophyseal System; Pituitary-Adrenal System; Puberty; Sex Characteristics; Brain
PubMed: 37422090
DOI: 10.1016/j.brainresbull.2023.110701