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Merck Frosst/CIHR Research Chair in Obesity, Centre de Recherche de l’Hôpital Laval, Hôpital Laval, 2725 Chemin Sainte-Foy, Québec, G1V 4G5 Canada

(Requests for offprints should be addressed to D Richard; Email: denis.richard{at}crhl.ulaval.ca)

The expression of genes encoding corticotropin-releasing factor (CRF) and its receptor type-1 (CRF₁R) and type-2 (CRF₂R) has been studied in the brain of rats with streptozotocin (STZ)-induced diabetes and adrenalectomy (ADX). Diabetic rats had a lower body weight compared to control rats. Food and water intake were increased in diabetic rats and decreased in ADX animals. The plasma corticosterone levels measured at the nadir of the circadian rhythm were significantly higher in diabetic rats compared to non-diabetic animals. STZ-diabetic rats demonstrated an induction of expression of CRF mRNA in the magnocellular part of the paraventricular hypothalamic nucleus (PVN) and in the supraoptic nucleus (SON), whereas the CRF transcript in the parvocellular PVN was significantly lower in rats with insulin deficiency. ADX strongly triggered the expression of CRF mRNA in the parvocellular neurons of the PVN in both non-diabetic and diabetic rats, and it decreased magnocellular CRF mRNA in diabetic animals. The expression of the CRF₁R in the parvocellular and magnocellular PVN and in the SON was induced by diabetes and decreased after ADX. The levels of the CRF₂R mRNA in the ventromedial hypothalamic nucleus (VMH) were significantly lower in diabetic rats without any noticeable effects of ADX. The present results suggest opposite effects of insulin and corticosterone deficiency on the hypophysiotropic CRF and the CRF₁R mRNA contents, whereas the expression of CRF₂R was mostly related to insulin, but not to the corticosterone status.

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