Neuroendocrine disruption of pubertal timing and interactions between homeostasis

The involvement of environmental factors such as endocrine disrupting chemicals
(EDCs) in the timing of onset of puberty is suggested by recent changes in age at
onset of puberty and pattern of distribution that are variable among countries,
as well as new forms of sexual precocity after migration. However, the evidence
of association between early or late pubertal timing and exposure to EDCs is weak
in humans, possibly due to heterogeneity of effects likely involving mixtures and
incapacity to assess fetal or neonatal exposure retrospectively. The
neuroendocrine system which is crucial for physiological onset of puberty is
targeted by EDCs. These compounds also act directly in the gonads and peripheral
sex-steroid sensitive tissues. Feedbacks add to the complexity of regulation so
that changes in pubertal timing caused by EDCs can involve both central and
peripheral mechanisms. In experimental conditions, several neuroendocrine
endpoints are affected by EDCs though only few studies including from our
laboratory aimed at EDC involvement in the pathophysiology of early sexual
maturation. Recent observations support the concept that EDC cause disturbed
energy balance and account for the obesity epidemic. Several aspects are linking
this system and the reproductive axis: coexisting neuroendocrine and peripheral
effects, dependency on fetal/neonatal programming and the many factors
cross-linking the two systems, for instance leptin, adiponectin, Agouti Related
Peptide (AgRP). This opens perspectives for future research and, hopefully,
measures preventing the disturbances of homeostasis caused by EDCs.