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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 -
International Journal of Epidemiology Oct 2023Early puberty timing is associated with adverse health outcomes. We aimed to examine prospective associations between objectively measured physical activity and puberty...
BACKGROUND
Early puberty timing is associated with adverse health outcomes. We aimed to examine prospective associations between objectively measured physical activity and puberty timing in boys and girls.
METHODS
In the UK Millennium Cohort Study, physical activity volume and intensities at 7 years were measured using accelerometers. Status of several pubertal traits and age at menarche were reported at 11, 14 and 17 years. Age at menarche in girls was categorized into tertiles. Other puberty traits were categorized into earlier or later than the median ages calculated from probit models, separately in boys and girls. Multivariable regression models, with adjustment for maternal and child characteristics including body mass index (BMI) at age 7 years as potential confounders, were performed to test the associations of total daily activity counts and fractions of activity counts across intensities (in compositional models) with puberty timing, separately in boys (n = 2531) and girls (n = 3079).
RESULTS
Higher total daily activity counts were associated with lower risks for earlier (vs later) growth spurt, body hair growth, skin changes and menarche in girls, and more weakly with lower risks for earlier skin changes and voice breaking in boys (odds ratios = 0.80-0.87 per 100 000 counts/day). These associations persisted on additional adjustment for BMI at 11 years as a potential mediator. No association with puberty timing was seen for any physical activity intensity (light, moderate or vigorous).
CONCLUSIONS
More physical activity regardless of intensity may contribute to the avoidance of earlier puberty timing, independently of BMI, particularly in girls.
Topics: Male; Child; Female; Humans; Cohort Studies; Puberty; Menarche; Body Mass Index; Accelerometry
PubMed: 37208864
DOI: 10.1093/ije/dyad063 -
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 -
Frontiers in Endocrinology 2023Noonan syndrome (NS) is a genetic multisystem disorder characterised by variable clinical manifestations including dysmorphic facial features, short stature, congenital...
BACKGROUND
Noonan syndrome (NS) is a genetic multisystem disorder characterised by variable clinical manifestations including dysmorphic facial features, short stature, congenital heart disease, renal anomalies, lymphatic malformations, chest deformities, cryptorchidism in males.
METHODS
In this narrative review, we summarized the available data on puberty and gonadal function in NS subjects and the role of the RAS/mitogen-activated protein kinase (MAPK) signalling pathway in fertility. In addition, we have reported our personal experience on pubertal development and vertical transmission in NS.
CONCLUSIONS
According to the literature and to our experience, NS patients seem to have a delay in puberty onset compared to the physiological timing reported in healthy children. Males with NS seem to be at risk of gonadal dysfunction secondary not only to cryptorchidism but also to other underlying developmental factors including the MAP/MAPK pathway and genetics. Long-term data on a large cohort of males and females with NS are needed to better understand the impact of delayed puberty on adult height, metabolic profile and well-being. The role of genetic counselling and fertility related-issues is crucial.
Topics: Male; Child; Adult; Female; Humans; Noonan Syndrome; Cryptorchidism; Gonads; Puberty; Mitogen-Activated Protein Kinases
PubMed: 37576960
DOI: 10.3389/fendo.2023.1213098 -
Endocrinology Jan 2021Puberty is a developmental period characterized by a broad range of physiologic changes necessary for the acquisition of adult sexual and reproductive maturity. These... (Review)
Review
Puberty is a developmental period characterized by a broad range of physiologic changes necessary for the acquisition of adult sexual and reproductive maturity. These changes mirror complex modifications within the central nervous system, including within the hypothalamus. These modifications result in the maturation of a fully active hypothalamic-pituitary-gonadal (HPG) axis, the neuroendocrine cascade ensuring gonadal activation, sex steroid secretion, and gametogenesis. A complex and finely regulated neural network overseeing the HPG axis, particularly the pubertal reactivation of gonadotropin-releasing hormone (GnRH) secretion, has been progressively unveiled in the last 3 decades. This network includes kisspeptin, neurokinin B, GABAergic, and glutamatergic neurons as well as glial cells. In addition to substantial modifications in the expression of key targets, several changes in neuronal morphology, neural connections, and synapse organization occur to establish mature and coordinated neurohormonal secretion, leading to puberty initiation. The aim of this review is to outline the current knowledge of the major changes that neurons secreting GnRH and their neuronal and glial partners undergo before and after puberty. Emerging mediators upstream of GnRH, uncovered in recent years, are also addressed herein. In addition, the effects of sex steroids, particularly estradiol, on changes in hypothalamic neurodevelopment and plasticity are discussed.
Topics: Gonadotropin-Releasing Hormone; Humans; Hypothalamus; Neuronal Plasticity; Neurons; Puberty
PubMed: 33175140
DOI: 10.1210/endocr/bqaa209 -
Brain Research Jan 2017Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental... (Review)
Review
Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental inputs and reorganization of cortical circuits that matches behavior with environmental contingencies. Significant headway has been achieved in characterizing and understanding sensitive period biology in primary sensory cortices, but relatively little is known about sensitive period biology in associative neocortex. One possible mediator is the onset of puberty, which marks the transition to adolescence, when animals shift their behavior toward gaining independence and exploring their social world. Puberty onset correlates with reduced behavioral plasticity in some domains and enhanced plasticity in others, and therefore may drive the transition from juvenile to adolescent brain function. Pubertal onset is also occurring earlier in developed nations, particularly in unserved populations, and earlier puberty is associated with vulnerability for substance use, depression and anxiety. In the present article we review the evidence that supports a causal role for puberty in developmental changes in the function and neurobiology of the associative neocortex. We also propose a model for how pubertal hormones may regulate sensitive period plasticity in associative neocortex. We conclude that the evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required. We argue that further work of this kind is urgently needed to determine how earlier puberty may negatively impact human health and learning potential. This article is part of a Special Issue entitled SI: Adolescent plasticity.
Topics: Animals; Humans; Neocortex; Neuronal Plasticity; Puberty; Sexual Maturation
PubMed: 27590721
DOI: 10.1016/j.brainres.2016.08.042 -
Seminars in Reproductive Medicine Mar 2019To understand the roles of kisspeptin and neurokinin B (NKB) in puberty and sex differences in their involvement, we conducted a series of experiments measuring the... (Review)
Review
To understand the roles of kisspeptin and neurokinin B (NKB) in puberty and sex differences in their involvement, we conducted a series of experiments measuring the release of gonadotropin-releasing hormone (GnRH) and kisspeptin in the median eminence of the hypothalamus in male and female monkeys throughout sexual development. Results indicate that kisspeptin-10 and the NKB agonist, senktide, stimulated GnRH release in males and females at the prepubertal and pubertal stages, but females are much more sensitive to kisspeptin signaling than males. Moreover, throughout the progress of puberty, major remodeling of kisspeptin and NKB signaling pathways for the regulation of GnRH release takes place. In females during puberty, reciprocal pathways (i.e., kisspeptin signaling mediated through NKB neurons and NKB signaling mediated through kisspeptin neurons) are established, to provide powerful and flexible mechanisms for GnRH neurosecretory activity necessary for complex female reproductive function in adulthood. By contrast, during puberty in males, reciprocal pathways are consolidated to a simpler kisspeptin-dominant signaling pathway. Nevertheless, in primates, both kisspeptin and NKB signaling are contributing factors for the pubertal increase in GnRH release, rather than initiating puberty.
Topics: Animals; Female; Gonadotropin-Releasing Hormone; Humans; Kisspeptins; Macaca mulatta; Male; Neurokinin B; Puberty; Sex Characteristics; Signal Transduction
PubMed: 31847024
DOI: 10.1055/s-0039-3400253 -
Annals of Medicine Mar 2015It was previously assumed that brown adipose tissue (BAT) is present in humans only for a short period following birth, the time in which mechanisms of generating heat... (Review)
Review
It was previously assumed that brown adipose tissue (BAT) is present in humans only for a short period following birth, the time in which mechanisms of generating heat by way of shivering are not yet developed. Although BAT is maximally recruited in early infancy, findings in recent years have led to a new consensus that metabolically active BAT remains present in most children and many adult humans. Evidence to date supports a slow and steady decline in BAT activity throughout life, with the exception of an intriguing spike in the prevalence and volume of BAT around the time of puberty that remains poorly understood. Because BAT activity is more commonly observed in individuals with a lower body mass index, an association seen in both adult and pediatric populations, there is the exciting possibility that BAT is protective against childhood and adult obesity. Indeed, the function and metabolic relevance of human BAT is currently an area of vigorous research. The goal of this review is to summarize what is currently known about changes that occur in BAT during various stages of life, with a particular emphasis on puberty and aging.
Topics: Adipose Tissue, Brown; Adipose Tissue, White; Adult; Aged; Aging; Animals; Female; Humans; Male; Middle Aged; Obesity; Puberty; Retrospective Studies; Thermogenesis
PubMed: 24888388
DOI: 10.3109/07853890.2014.914807 -
Frontiers in Endocrinology 2022Puberty is a critical process characterized by several physical and psychological changes that culminate in the achievement of sexual maturation and fertility. The onset... (Review)
Review
Puberty is a critical process characterized by several physical and psychological changes that culminate in the achievement of sexual maturation and fertility. The onset of puberty depends on several incompletely understood mechanisms that certainly involve gonadotropin-releasing hormone (GnRH) and its effects on the pituitary gland. The role of makorin ring finger protein 3 (MKRN3) in the regulation of pubertal timing was revealed when loss-of-function mutations were identified in patients with central precocious puberty (CPP), which to date, represent the most commonly known genetic cause of this condition. The gene showed ubiquitous expression in tissues from a broad spectrum of species, suggesting an important cellular role. Its involvement in the initiation of puberty and endocrine functions has just begun to be studied. This review discusses some of the recent approaches developed to predict MKRN3 functions and its involvement in pubertal development.
Topics: Gonadotropin-Releasing Hormone; Humans; Puberty; Puberty, Precocious; Ribonucleoproteins; Ubiquitin-Protein Ligases
PubMed: 36187104
DOI: 10.3389/fendo.2022.991322 -
Frontiers in Neuroendocrinology Jan 2015Substantial progress has been made in recent years toward deciphering the molecular and genetic underpinnings of the pubertal process. The availability of powerful new... (Review)
Review
Substantial progress has been made in recent years toward deciphering the molecular and genetic underpinnings of the pubertal process. The availability of powerful new methods to interrogate the human genome has led to the identification of genes that are essential for puberty to occur. Evidence has also emerged suggesting that the initiation of puberty requires the coordinated activity of gene sets organized into functional networks. At a cellular level, it is currently thought that loss of transsynaptic inhibition, accompanied by an increase in excitatory inputs, results in the pubertal activation of GnRH release. This concept notwithstanding, a mechanism of epigenetic repression targeting genes required for the pubertal activation of GnRH neurons was recently identified as a core component of the molecular machinery underlying the central restraint of puberty. In this chapter we will discuss the potential contribution of various mechanisms of epigenetic regulation to the hypothalamic control of female puberty.
Topics: Animals; Epigenesis, Genetic; Female; Gonadotropin-Releasing Hormone; Humans; Hypothalamus; Neurons; Puberty; Sexual Maturation
PubMed: 25171849
DOI: 10.1016/j.yfrne.2014.08.003