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Laboratoire de Neuroendocrinologie du Développement, UPRES-EA 2701, Université de Lille 1, 59655 Villeneuve d’Ascq, France; INSERM, U-457 (B.Bl., B.Br.), 75019 Paris; and INSERM, U-501 (M.G.), 13916 Marseilles, France
Address all correspondence and requests for reprints to: Dr. J. Lesage, Laboratoire de Neuroendocrinologie du Développement, UPRES-EA 2701, Université de Lille 1, Bât. SN4, 59655 Villeneuve d’Ascq, France. E-mail: Jean.Lesage{at}pop.univ-lille1.fr
As fetal overexposure to glucocorticoids has been postulated to induce intrauterine growth retardation (IUGR) in humans, we investigated the effects of maternal 50% food restriction (FR50) in rats during the last week of gestation on the hypothalamo-pituitary adrenal (HPA) axis activity in both mothers and their fetuses. In mothers, FR50 increased both the plasma corticosterone (B) level from embryonic days 19–21 and the relative adrenal weight at term. FR50 decreased at term both the maternal plasma corticosteroid-binding globulin level and placental 11ß-hydroxysteroid dehydrogenase type 2 expression. In newborns, maternal FR50 reduced body and adrenal weights, glucocorticoid and mineralocorticoid receptor expressions in the hippocampus, corticoliberin expression in the hypothalamic paraventricular nucleus, and plasma ACTH. In FR50 newborns, the plasma B level was increased at birth and decreased 2 h later. When maternal circulating B was maintained at the basal level by adrenalectomy and B supply, FR50 induced IUGR in pups and decreased placental 11ß- hydroxysteroid dehydrogenase type 2 expression at term, but did not disturb the offspring’s HPA axis. These results suggest that maternal undernutrition during late gestation induces both IUGR and an overexposure of fetuses to maternal B, which disturb the development of the HPA axis.
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