ISSN 1662-4009 (Online)

ESPE Yearbook of Paediatric Endocrinology (2019) 16 7.10 | DOI: 10.1530/ey.16.7.10

Is there a causal relationship between obesity and puberty?

Reinehr T & Roth CL

To read the full abstract: Lancet Child Adolesc Health. 2019 Jan;3(1):44–54.

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.

References: 1. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman-Giddens ME. 2001 Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics 108: 347–53.

2. Wang Y. 2002 Is obesity associated with early sexual maturation? A comparison of the association in American boys versus girls. Pediatrics 110: 903–10.

3. Reinehr T, Bosse C, Lass N, Rothermel J, Knop C, Roth CL. 2017 Effect of weight loss on puberty onset in overweight children. J. Pediatr. 184: 143–150.

4. Casanueva FF, Dieguez C. 1999 Neuroendocrine regulation and actions of leptin. Front. Neuroendocrinol. 20: 317–63.

5. Navarro VM, Castellano JM, Garcia-Galiano D, Tena-Sempere M. 2007 Neuroendocrine factors in the initiation of puberty: the emergent role of kisspeptin. Rev. Endocr. Metab. Disord. 8: 11–20.

6. Rutters F, Nieuwenhuizen AG, Verhoef SP, Lemmens SG, Vogels N, Westerterp-Platenga MS. 2009 The relationship between leptin, gonadotropic hormones, and body composition during puberty in a Dutch children cohort. Eur. J. Endocrinol. 160: 973–78.

7. Sorensen K, Aksglaede L, Munch-Andersen T, Munch-Andersen T, Aachmann-Andersen NJ, Petersen JH, Hilsted L, Helge JW, Juul A. Sex hormone-binding globulin levels predict insulin sensitivity, disposition index, and cardiovascular risk during puberty. Diabetes Care 2009; 32: 909–14.

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