| First Author | Chen HL | Year | 1994 |
| Journal | Am J Physiol | Volume | 266 |
| Issue | 3 Pt 1 | Pages | E427-32 |
| PubMed ID | 8166263 | Mgi Jnum | J:17505 |
| Mgi Id | MGI:65542 | Doi | 10.1152/ajpendo.1994.266.3.E427 |
| Citation | Chen HL, et al. (1994) Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis. Am J Physiol 266(3 Pt 1):E427-32 |
| abstractText | A single intracerebroventricular injection of dexamethasone rapidly (within 30 min) decreases brown adipose tissue thermogenesis by 25% as assessed by GDP binding and increases plasma insulin twofold in adrenalectomized ob/ob mice. The present study investigated the type of corticoid receptor(s) that mediate these effects and determined whether protein synthesis was necessary for expression of these glucocorticoid actions in ob/ob mice. Intracerebroventricular injection of aldosterone (a type I-corticoid receptor agonist) was ineffective in altering peripheral metabolism in adrenalectomized ob/ob mice, whereas RU-486 (a type II-corticoid receptor antagonist) abolished the effects of dexamethasone. Thus type II-like corticoid receptors, not type I receptors, mediated the rapid effects of dexamethasone in adrenalectomized ob/ob mice. Anisomycin (0.5 mg) administered subcutaneously almost completely suppressed (-92%) cerebral protein synthesis, but anisomycin did not abolish the rapid effects of dexamethasone in adrenalectomized ob/ob mice. Thus protein synthesis is not a prerequisite for rapid effects of dexamethasone in adrenalectomized ob/ob mice. |
