Inhibition of gold thioglucose lesion formation in the ventromedial hypothalamus by a glucocorticoid.
A single intraperitoneal injection of gold thioglucose (GTG) yields a lesion in the ventromedial hypothalamus (VMH), eventually producing obesity. The anti-inflammatory compounds, aspirin or glucocorticoid (GC), have been shown previously to block GTG lesion formation in the VMH when examined at the light microscopic level. Ultramicroscopic changes in the VMH have been observed to account for the inhibition of GTG-induced lesions with aspirin. We sought to determine whether or not GC action in the prevention of GTG lesion formation was also accompanied by VMH morphological changes at the ultrastructural level. Our results demonstrated that hydrocortisone pretreatment completely protected the VMH from any GTG-induced necrosis. We hypothesize that this inhibition of GTG lesion formation is not mediated by GC anti-inflammatory activity, but related to an anti-insulin activity of GC, GC-induced changes in VMH cell membrane receptor function, and/or alterations in serotonin metabolism.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D006051:Aurothioglucose / Q000037:antagonists & inhibitors*; D005260:Female; D006046:Gold / Q000037:antagonists & inhibitors*; D006854:Hydrocortisone / Q000494:pharmacology*; D007033:Hypothalamus, Middle / Q000187:drug effects* / Q000648:ultrastructure; D007329:Insulin Antagonists; D051379:Mice; D008854:Microscopy, Electron; D011965:Receptors, Glucocorticoid / Q000187:drug effects; D012701:Serotonin / Q000378:metabolism
D007329:Insulin Antagonists; D011965:Receptors, Glucocorticoid; D006051:Aurothioglucose; D012701:Serotonin; D006046:Gold; D001241:Aspirin; D006854:Hydrocortisone