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  • Title: Modulation of urocortin-induced hypophagia and weight loss by corticotropin-releasing factor receptor 1 deficiency in mice.
    Author: Bradbury MJ, McBurnie MI, Denton DA, Lee KF, Vale WW.
    Journal: Endocrinology; 2000 Aug; 141(8):2715-24. PubMed ID: 10919255.
    Abstract:
    Intracerebroventricular injection of CRF or urocortin (Ucn) reduces appetite and body weight. CRFR1 and CRFR2, the receptors for CRF and Ucn, are expressed in neurons associated with appetite-control and metabolism, but their relative contributions in mediating CRF- or Ucn-induced hypophagia and weight loss are not known. We used homozygous mice lacking CRFR1 (CRFR1-/-) and wild-type littermates to determine the role of CRFR1 in mediating the changes in food intake and body weight following intracerebroventricular administration of Ucn. CRFR1-/- mice, which are glucocorticoid deficient, were given corticosterone in their drinking water to induce diurnal variations in circulating corticosterone. A 7-day intracerebroventricular infusion of Ucn transiently suppressed ad libitum food intake equally in CRFR1-/- and wild-type mice. Body weight reduction during Ucn infusion paralleled food intake in wild-type mice, but persisted throughout the infusion in CRFR1-/- mice. After food-deprivation, acute intracerebroventricular injection of Ucn suppressed food intake for 1.5 h in wild-type mice. By contrast, CRFR1-/- mice did not respond to Ucn 1.5 h after injection. At later time points, Ucn suppressed food intake equally in both genotypes. The distinct time courses of CRF-receptor-induced hypophagia suggest that separate pathways act cooperatively to adjust food intake during challenges to homeostasis.
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