Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia.

Abstract The role of beta-adrenoreceptors in modulating feeding in glucoprivation- and lipoprivation-induced hyperphagias was studied in rats by measuring the efficacy of the selective beta 2 -adrenoreceptor agonist salbutamol to antagonize the hyperphagic response induced by injection of 2-deoxy- d -glucose (2-DG), insulin, or sodium mercaptoacetate (MA). 2-DG and insulin are blockers of glucose utilization, and their administration stimulates receptor cells that are selectively sensitive to central glucose availability. MA stimulates feeding in rats maintained on a fat-supplemented diet, by blocking fatty acid oxidation at different levels in the metabolic pathway. We found that salbutamol dose-dependently antagonized both the insulin- and MA-induced hyperphagia, with reductions in food intake up to 100% compared with rats treated with insulin or MA alone. On the contrary, salbutamol, even at the highest dose (15 mg/kg, IP), was completely ineffective against 2-DG-induced hyperphagia. The present results support the previously proposed notion that there are different neuronal or humoral circuits underlying the hyperphagic responses to the metabolic stimuli induced by glucoprivation (i.e., 2-DG and insulin administration), and they extend our knowledge on the effects of salbutamol on glucoprivic and lipoprivic control of feeding.