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Am J Physiol Endocrinol Metab 281: E592-E599, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 3, E592-E599, September 2001

Glucocorticoids impair fetal beta -cell development in rats

B. Blondeau1, J. Lesage2, P. Czernichow1, J. P. Dupouy2, and B. Bréant1

1 Institut National de la Santé et de la Recherche Médicale Unité 457, Hôpital Robert Debré, Paris; and 2 Unité Propre de Recherche de l'Enseignement Superieur Equipe d'Accueil, EA 2701, University of Lille 1, Lille, France

In rats, poor fetal growth due to maternal food restriction during pregnancy is associated with decreased beta -cell mass at birth and glucose intolerance in adulthood. Overexposure to glucocorticoids in utero can induce intrauterine growth retardation in humans and animals and subsequent glucose intolerance in rodents. The aims of this study were to investigate whether glucocorticoid overexposure mediates the effect of undernutrition on beta -cell mass and to study their potential role in normally nourished rats. Undernutrition significantly increased maternal and fetal corticosterone levels. Twenty-one-day-old fetuses with undernutrition showed growth retardation and decreased pancreatic insulin content; adrenalectomy and subcutaneous corticosterone implants in their dams prevented the maternal corticosterone increase and restored fetal beta -cell mass. In fetuses with normal nutrition, fetal corticosterone levels were negatively correlated to fetal weight and insulin content; fetal beta -cell mass increased from 355 ± 48 µg in sham to 516 ± 160 µg after maternal adrenalectomy; inhibition of steroid production by metyrapone induced a further increase to 757 ± 125 µg. Our data support the new concept of a negative role of glucocorticoids in fetal beta -cell development.

undernutrition; pancreatic beta -cell; morphometry; fetal environment


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