While there are many theories on the control of feeding behavior that emphasize a role for energy substrates and their metabolism, the mechanism that couples changes in energy substrate supply and metabolism to alterations in food intake remains unclear. The purpose of the present project was to investigate the possibility that central ATP-sensitive potassium (KATP(+)) channels may serve as integrators between cellular energetics and alterations in neuronal activity that control feeding, such that pharmacologic manipulation of the channels would result in alterations in feeding behavior. Intracerebroventricular (ICV) injections of the KATP(+) channel blocker glibenclamide significantly increased feeding in fasted and fed male Sprague-Dawley rats. Likewise, the first generation sulfonylurea, tolbutamide, also increased feeding. ICV injection of the KATP(+) channel opener, diazoxide, modestly inhibited feeding. These results suggest that central KATP(+) channels may be involved in the regulation of feeding behavior.
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