The Metabolic Programming of Pubertal Onset.

BACKGROUND

There is increasing evidence that maternal factors such as nutritional status (both under and over-nutrition) and diabetes, alongside prenatal exposure to endocrine disrupting chemicals (EDCs), are associated with early pubertal onset in offspring. Such children are also at increased risk of the metabolic syndrome during adolescence and young adulthood.

AIM

This literature review focuses on the role of the prenatal environment in programming pubertal onset, and the impact of prenatal metabolic stressors on the declining average age of puberty.

METHOD

A review of all relevant literature was conducted in PubMed by the authors.

OUTCOME

The mechanism for this appears to be mediated through metabolic signals, such as leptin and insulin, on the kisspeptin-neuronal nitric oxide-gonadotropin releasing hormone (KiNG) axis. Exposed children have an elevated risk of childhood obesity and display a phenotype of hyperinsunlinaemia and hyperleptinaemia. These metabolic changes permit an earlier attainment of the nutritional "threshold" for puberty. Unfortunately, this cycle may be amplified across subsequent generations, however early intervention may help "rescue" progression of this programming.