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Submitted on November 7, 2003
Accepted on December 18, 2003
1 Service of Endocrinology, Department of Medicine, Faculty of Medicine, Université de Sherbrooke, Sherbrooke Quebec, Department of Psychiatry, McGill University, Douglas Hospital Research Center, Montreal, Canada
* To whom correspondence should be addressed. E-mail: waldom{at}douglas.mcgill.ca.
Previous studies have shown that leptin can regulate the adrenocortical axis. Neonatal rodents exhibit a period of adrenal hyporesponsiveness to stress in the first 2 weeks of life and we determined the role of leptin as a mediator of this process. We examined the direct effects of leptin on neonatal adrenal steroidogenic responses to ACTH under basal conditions and after 24 h maternal separation. In isolated adrenocortical cells from as early as postnatal day (PND) 5 and throughout the neonatal period, acute (2h30) incubation with leptin significantly inhibited ACTH-stimulated corticosterone and aldosterone secretion, without affecting cAMP production. In PND10 pups, 24 h maternal separation and the resulting rapid decline in plasma leptin levels increased basal corticosterone and aldosterone secretion in vivo and in isolated cells, but did not modify the ability of leptin to inhibit stimulated steroid production in vitro. Maternal separation in PND10 pups increased adrenal expression of StAR and PBR proteins as well as all steroidogenic enzymes measured (3
-HSD, P450C11B1 and P450C11B2). Leptin (1 mg/kg bw, ip) replacement during maternal separation did not affect basal corticosterone output, but reduced corticosterone secretion, StAR and PBR expression induced by exogenous ACTH challenge (20 or 80 ug/kg bw, ip). These results indicate that leptin inhibits ACTH-stimulated secretion of corticosterone and aldosterone at least through a rapid reduction in the expression of StAR and PBR protein in the neonatal adrenal gland. Since leptin concentrations in pups are controlled to a large extent by maternal diet, these results emphasize the key role of leptin to mediate the maternal influence on the adrenocortical axis of the infant.
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