Disruption of feeding behavior in CRH receptor I-deficient mice is dependent on glucocorticoids

Corticotropin-releasing hormone (CRH) has been found to markedly suppress f ood intake and reduce body weight. However, it still remains to be clarifie d whether those effects are mediated via either the CRH receptor 1 (CRHR1) or the CRH receptor 2 (CRHR2), or both receptor subtypes. Therefore, we inv estigated whether CRHR1-deficient mice (CRHR1-KO) show abnormalities in bod y weight and feeding behavior. CRHR1-KO and wildtype mice showed no differe nce in the total amount of food intake. However, there was a significant di sruption in the circadian distribution of food intake: CRHR1 mutants consum ed significantly more food during the light period (P < 0.01). The normal d iurnal pattern could be completely restored by oral administration of corti costerone 21-sulfate (5 mg/l added to the water-based liquid diet). We ther efore conclude that in CRHR1-KO mice, the disruption of feeding behavior mi ght be causally related to glucocorticoid deficiency, but that the CRHR1 is not likely to play a critical role in the basal regulation of ingestive be havior. NeuroReport 11:1963-1966 (C) 2000 Lippincott Williams & Wilkins.