| First Author | Bradbury MJ | Year | 2000 |
| Journal | Endocrinology | Volume | 141 |
| Issue | 8 | Pages | 2715-24 |
| PubMed ID | 10919255 | Mgi Jnum | J:65561 |
| Mgi Id | MGI:1926739 | Doi | 10.1210/endo.141.8.7606 |
| Citation | Bradbury MJ, et al. (2000) Modulation of urocortin-induced hypophagia and weight loss by corticotropin-releasing factor receptor 1 deficiency in mice [see comments]. Endocrinology 141(8):2715-24 |
| abstractText | 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. |
