anisomycin has been researched along with Obesity* in 2 studies
2 other study(ies) available for anisomycin and Obesity
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Dexamethasone regulates obese expression in isolated rat adipocytes.
An obese (ob) gene product, expressed specifically in adipose tissues, regulates energy balance. Here we report adipocytes in adipose tissue actually express ob mRNA and that a synthetic glucocorticoid (dexamethasone) regulates expression of the ob gene. Addition of 100 nM dexamethasone to isolated rat adipocytes rapidly induced a 4-8 fold increase in ob mRNA. This increase in ob mRNA level was apparent within 1 h, and reached a maximum at about 7 h after stimulation. The dexamethasone-stimulated increase of ob mRNA was only partially blocked by protein synthesis inhibitors cycloheximide (20 micrograms/ml) or anisomycin (200 microM). This suggests that new protein synthesis is not necessarily required for the observed dexamethasone-stimulated increase in ob mRNA. Topics: 1-Methyl-3-isobutylxanthine; 3T3 Cells; Adipocytes; Adipose Tissue; Adipose Tissue, Brown; Animals; Anisomycin; Cell Differentiation; Cells, Cultured; Cycloheximide; Dexamethasone; Epididymis; Gene Expression; Male; Mice; Muscle, Smooth, Vascular; Obesity; Protein Synthesis Inhibitors; Rats; Rats, Sprague-Dawley; RNA, Messenger | 1995 |
Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis.
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. Topics: Adipose Tissue, Brown; Adrenalectomy; Animals; Anisomycin; Brain; Dexamethasone; Guanosine Diphosphate; Insulin; Male; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Mifepristone; Obesity; Oxygen Consumption; Protein Biosynthesis; Receptors, Glucocorticoid | 1994 |