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The Metabolic Programming of Pubertal Onset

Clinton Roddick1, Mark Harris1, Paul L Hofman2

  • 1Department of Endocrinology and Diabetes, Queensland Children's Hospital, Brisbane, Queensland, Australia.

Clinical Endocrinology
|October 3, 2024
PubMed

Insights

Maternal factors like nutrition and endocrine disruptors can trigger early puberty by affecting metabolic signals. This can increase the risk of metabolic syndrome in offspring, potentially impacting future generations.

Area of Science:

  • Reproductive endocrinology
  • Developmental biology
  • Environmental health

Background:

  • Maternal nutrition (under/over-nutrition) and diabetes are linked to early pubertal onset.
  • Prenatal exposure to endocrine-disrupting chemicals (EDCs) is associated with early puberty.
  • Children with early puberty face increased risk of metabolic syndrome in adolescence and young adulthood.

Purpose of the Study:

  • To review the role of the prenatal environment in programming pubertal onset.
  • To examine the impact of prenatal metabolic stressors on the declining average age of puberty.

Main Methods:

  • A comprehensive literature review was conducted.
  • Relevant studies were identified through PubMed searches.

Main Results:

  • Metabolic signals (leptin, insulin) on the kisspeptin-neuronal nitric oxide-gonadotropin releasing hormone (KiNG) axis mediate early puberty.
  • Prenatal exposures increase offspring risk of childhood obesity, hyperinsulinemia, and hyperleptinemia.
  • These metabolic changes facilitate earlier attainment of the pubertal "threshold."

Conclusions:

  • The prenatal environment significantly influences pubertal timing.
  • Early pubertal onset due to metabolic programming may increase long-term health risks.
  • Interventions may help mitigate the generational amplification of these programming effects.
Abstract

Keywords:
childhood obesityinsulinkisspeptinleptinmetabolic syndromeprenatal exposurepuberty

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