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Early Neuroendocrine Disruption in Hypothalamus and Hippocampus: Developmental Effects Including Female Sexual Maturation and Implications for Endocrine Disrupting Chemical Screening
Author(s) -
Bourguig J.P.,
Franssen D.,
Gérard A.,
Janssen S.,
Pinson A.,
Naveau E.,
Parent A.S.
Publication year - 2013
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12107
Subject(s) - medicine , endocrinology , hypothalamus , precocious puberty , endocrine system , biology , sexual maturity , diethylstilbestrol , stimulation , toxicant , hormone , toxicity
The timing of puberty has been mainly studied in females for several reasons, including the possible evaluation of a precise timer (i.e. menarcheal age) and concerns with respect to the high prevalence of precocity in females as opposed to males. Human evidence of altered female pubertal timing after exposure to endocrine disrupting chemicals ( EDC s) is equivocal. Among the limiting factors, most studies evaluate exposure to single EDC s at the time of puberty and hardly assess the impact of lifelong exposure to mixtures of EDC s. Some rodent and ovine studies indicate a possible role of foetal and neonatal exposure to EDC s, in accordance with the concept of an early origin of health and disease. Such effects possibly involve neuroendocrine mechanisms because the hypothalamus is a site where homeostasis of reproduction, as well as control of energy balance, is programmed and regulated. In our previous studies, pulsatile g onadotrophin‐ r eleasing h ormone ( G n RH ) secretion control via oestrogen, glutamate and aryl hydrocarbon receptors was shown to be involved in the mechanism of sexual precocity after early postnatal exposure to the insecticide dichlorodiphenyltrichloroethane. Very recently, we have shown that neonatal exposure to the potent synthetic oestrogen diethylstilbestrol ( DES ) is followed by early or delayed puberty depending on the dose, with consistent changes in developmental increase of G n RH pulse frequency. Moreover, DES results in reduced leptin stimulation of G n RH secretion in vitro , an effect that is additive with prenatal food restriction. Thus, using puberty as an endpoint of the effects of EDC , it appears necessary to consider pre‐ and perinatal exposure to low doses and to pay attention to the other conditions of prenatal life, such as energy availability, keeping in mind the possibility that puberty could not only be advanced, but also delayed through neuroendocrine mechanisms.