The Metabolic Programming of Pubertal Onset
Study context
- Population
- Offspring exposed to prenatal metabolic stressors (maternal under/over-nutrition, diabetes, endocrine disrupting chemicals (EDCs))
- Outcome
- Prenatal programming of pubertal onset
Methodological detailsReview of all relevant literature in PubMed
- Review of all relevant literature in PubMed
Main finding
As reported in the abstract
- Mechanism appears mediated through metabolic signals (leptin, insulin) on the kisspeptin-neuronal nitric oxide-GnRH (KiNG) axis
- Exposed children have elevated risk of childhood obesity and a phenotype of hyperinsulinaemia and hyperleptinaemia
- These metabolic changes permit earlier attainment of the nutritional threshold for puberty
- Cycle may be amplified across subsequent generations; early intervention may help rescue progression of this programming
Original publication
The Metabolic Programming of Pubertal Onset. Clin Endocrinol (Oxf). Published 3 October 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →