AJP - Endocrinology and Metabolism, Vol 266, Issue 3 E427-E432, Copyright © 1994 by American Physiological Society
Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis
H. L. Chen and D. R. Romsos
Department of Food Science and Human Nutrition, Michigan State University, East Lansing 48824-1224.
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.
