To read the full abstract: Lancet Child Adolesc Health. 2019 Jan;3(1):4454.
This article reviews cross-sectional, longitudinal and intervention studies regarding the bidirectional relationship between obesity and puberty.
An increasing prevalence of obesity amongst children and adolescents is reported globally. Epidemiological cross-sectional and longitudinal studies consistently show that obese girls tend to enter puberty earlier than non-obese girls (1, 2). The situation appears more complex in boys: overweight boys mature earlier, but obese boys mature later (2). In intervention studies, reduction in BMI-SDS reduced the likelihood of puberty onset in the next year in overweight and obese girls, but increased this likelihood in overweight and obese boys (3). Of interest, onset of puberty was associated with an increase of gonadotropins, suggesting a normal hypothalamic-pituitary initiation of puberty.
The authors summarize the hypotheses for the relationship between obesity and puberty timing, and the sex differences. The most promising link is the adipokine leptin and its interaction with the kisspeptin system. Indeed, adipose tissue acts as an endocrine organ secreting adipokines, such as leptin, which stimulates GnRH by activating kisspeptin neurons (4, 5). Interestingly, leptin regulation of puberty is sex-specific: testosterone inhibits leptin secretion from adipocytes (6). This sex difference might explain why the onset of puberty shifts to an earlier age in obese girls, but to a later age in obese boys. Peripheral mechanisms, such as adipose tissue aromatase activity, could also influence the timing of puberty. Finally, puberty is also influenced by insulin resistance associated with obesity: hyperinsulinemia reduces sex hormone binding globulin concentrations and thus increases the bioavailability of sex steroids (7). In addition, prenatal and childhood nutrition, physical activity or endocrine disrupting chemicals are potential mediators linking obesity to puberty timing.
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