VMH obesity reduced but not reversed by scopolamine methyl nitrate.
Chronic administration of scopolamine methyl nitrate, at doses much greater than required to block vagally mediated insulin secretion, reduced static phase VMH obesity by only 31%. At least 59% of the obesity persisted even when the initially effective dose (0.15 mg/Kg, 4 times/day) was increased eight-fold. The larger dose also did not prevent VMH hyperphagia and weight gain when scopolamine treatment was begun before the lesion. By ten days after the lesion, reduced gastrointestinal motility apparently prevented further weight gain. These results suggest that much of the obesity caused by VMH lesions is independent of vagally mediated insulin secretion or other excess vagal efferent activity. The doses used in this experiment were large in order to provide strong evidence for this conclusion.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects*; D004435:Eating / Q000187:drug effects; D005260:Female; D005769:Gastrointestinal Motility / Q000187:drug effects; D007031:Hypothalamus / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000502:physiology*; D007328:Insulin / Q000097:blood; D051381:Rats; D011976:Receptors, Muscarinic / Q000187:drug effects; D012602:Scopolamine Derivatives / Q000494:pharmacology*
D001786:Blood Glucose; D007328:Insulin; D011976:Receptors, Muscarinic; D012602:Scopolamine Derivatives