Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis.
Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis.
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CNS 中的 II 型糖皮质激素受体调节 ob/ob 小鼠的代谢,不依赖于蛋白质合成。
DOI:
10.1152/ajpendo.1994.266.3.e427
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发表时间:
1994
期刊:
影响因子:
--
通讯作者:
Romsos,DR
中科院分区:
文献类型:
--
作者:
Chen,HL;Romsos,DR
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.