Puberty: Normal physiology (brief overview)

Wood, Claire; Lane, Laura C; Cheetham, Tim

doi:10.1016/j.beem.2019.03.001

Cited by 96 publications

(84 citation statements)

References 55 publications

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“…Puberty is an intricate physiological process regarded as the transition from childhood to sexual maturity that develops in a defined period of time ( Plant, 2015 ; Sisk and Foster, 2004 ; Terasawa and Fernandez, 2001 ; Wood et al, 2019 ). It begins with increased activity of the hypothalamic-pituitary-gonadal (HPG) axis induced by stimulation of gonadotropin-releasing hormone (GnRH) neurons ( Han et al., 2005 ; Plant, 2015 ; Sisk and Foster, 2004 ).…”

Section: Introductionmentioning

confidence: 99%

Hypothalamic and Cell-Specific Transcriptomes Unravel a Dynamic Neuropil Remodeling in Leptin-Induced and Typical Pubertal Transition in Female Mice

et al. 2020

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Summary Epidemiological and genome-wide association studies (GWAS) have shown high correlation between childhood obesity and advance in puberty. Early age at menarche is associated with a series of morbidities, including breast cancer, cardiovascular diseases, type 2 diabetes, and obesity. The adipocyte hormone leptin signals the amount of fat stores to the neuroendocrine reproductive axis via direct actions in the brain. Using mouse genetics, we and others have identified the hypothalamic ventral premammillary nucleus (PMv) and the agouti-related protein (AgRP) neurons in the arcuate nucleus (Arc) as primary targets of leptin action in pubertal maturation. However, the molecular mechanisms underlying leptin's effects remain unknown. Here we assessed changes in the PMv and Arc transcriptional program during leptin-stimulated and typical pubertal development using overlapping analysis of bulk RNA sequecing, TRAP sequencing, and the published database. Our findings demonstrate that dynamic somatodendritic remodeling and extracellular space organization underlie leptin-induced and typical pubertal maturation in female mice.

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Section: Introductionmentioning

confidence: 99%

Hypothalamic and Cell-Specific Transcriptomes Unravel a Dynamic Neuropil Remodeling in Leptin-Induced and Typical Pubertal Transition in Female Mice

et al. 2020

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“…The etiology of delayed puberty in NI patients may be multifactorial (1, 2, 14), but in our small study population a causative factor was not identified. However, it is known that secondary chronic malnutrition reported in these patients (6) largely contributes to their delayed initiation of pubertal development.…”

Section: Discussionmentioning

confidence: 57%

“…Puberty onset for individuals living in relatively similar conditions, is characterized by a 4–5 years physiological variation in sexual maturation (1–3), and is expected to occur between 8–13 and 9–14 years of age, respectively, in girls and boys (2).…”

Section: Discussionmentioning

confidence: 99%

“…Brain malformation associated with pituitary dysfunction can also be considered (19). However, the role of genetic factors and fetal programming should not be excluded (1–3).…”

Section: Discussionmentioning

confidence: 99%

“…Puberty is a physiologic process marked by the appearance of secondary sex characteristics (1). The absence of sexual maturation signs at 2–2.5 standard deviations or more than the mean age (ca.…”

Section: Introductionmentioning

confidence: 99%

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Disorders of Puberty in Severely Neurologically Impaired Children: Is Delayed Puberty an Underestimated Problem?

et al. 2019

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Introduction: In children with disabilities, precocious puberty (PP) has been reported, however there is a paucity of studies on delayed puberty (DP) in neurologically impaired (NI) children.Patients and Methods: We retrospectively evaluated 65 patients with severe disabilities (6–18 years). DP was considered whenever the following criteria where satisfied, respectively, for girls and boys, absence of breast development by age 13 or menarche by age 15, absence of at least 4 mL testicular growth volume or 2.5 cm length by age 14. PP was defined as the presence of puberty signs at <8 and 9 years of age, respectively, for girls and boys. In all patients, a physical examination was performed and a family history of DP was obtained. A hormonal panel was evaluated when puberty disorders were detected. As a control group we evaluated 50 age-matched healthy subjects.Results: Puberty disorders were observed in 12 NI patients and in one control (18.5 vs. 2%, p < 0.01). DP was detected in 8 NI subjects (3M/5F) and in one healthy boy (p = 0.04), without differences between genders among patients from the NI group (p = 0.2), and compared with the controls (p = 0.4). In five of the eight NI subjects, Tanner stage 1 was observed; in three subjects adrenarche was present without pubertal progression for more than 2 years. Low levels of gonadotropins were detected in all NI subjects with DP. The number of subjects with a BMI <-3SDS was higher in NI patients with DP compared to NI subjects with normal puberty (p < 0.01); normal weight was detected in one healthy boy. The family history for pubertal delay was negative in all NI patients with DP and positive in the control subject.Conclusion: NI children and adolescents may experience delayed pubertal changes. An endocrinological follow-up with pubertal development monitoring is strongly recommended in order to evaluate whether targeted interventions may improve outcomes.

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Trace elements as potential modulators of puberty‐induced amelioration of oxidative stress and inflammation in childhood obesity

et al. 2023

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Although puberty is known to influence obesity progression, the molecular mechanisms underlying the role of sexual maturation in obesity‐related complications remains largely unexplored. Here, we delve into the impact of puberty on the most relevant pathogenic hallmarks of obesity, namely oxidative stress and inflammation, and their association with trace element blood status. To this end, we studied a well‐characterized observational cohort comprising prepubertal (N = 46) and pubertal (N = 48) children with obesity. From all participants, plasma and erythrocyte samples were collected and subjected to metallomics analysis and determination of classical biomarkers of oxidative stress and inflammation. Besides the expected raise of sexual hormones, pubertal children displayed better inflammatory and oxidative control, as reflected by lower levels of C‐reactive protein and oxidative damage markers, as well as improved antioxidant defense. This was in turn accompanied by a healthier multielemental profile, with increased levels of essential elements involved in the antioxidant system and metabolic control (metalloproteins containing zinc, molybdenum, selenium, and manganese) and decreased content of potentially deleterious species (total copper, labile free iron). Therefore, our findings suggest that children with obesity have an exacerbated inflammatory and oxidative damage at early ages, which could be ameliorated during pubertal development by the action of trace element‐mediated buffering mechanisms.

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Puberty: Normal physiology (brief overview)

Cited by 96 publications

References 55 publications

Hypothalamic and Cell-Specific Transcriptomes Unravel a Dynamic Neuropil Remodeling in Leptin-Induced and Typical Pubertal Transition in Female Mice

Hypothalamic and Cell-Specific Transcriptomes Unravel a Dynamic Neuropil Remodeling in Leptin-Induced and Typical Pubertal Transition in Female Mice

Disorders of Puberty in Severely Neurologically Impaired Children: Is Delayed Puberty an Underestimated Problem?

Trace elements as potential modulators of puberty‐induced amelioration of oxidative stress and inflammation in childhood obesity

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