Hepatic versus cerebral origin of stimulus for feeding induced by 2-deoxy-{d}-glucose in rats.

Abstract

Administration (i.v.) of 2-deoxy-D-glucose (2-DG), a competitive inhibitor of glucose utilization, increased the food intake of rats. Infusions of glucose or mannose abolished this effect, whereas equimolar fructose solutions did not affect 2-DG-induced feeding. Similar results were obtained when 2-DG and the hexoses were administered into the hepatic portal vein. The elicited feeding was due to glucoprivation at a site that is inaccessible to fructose. This site is likely to be in the brain, not the liver, because all 3 sugars can nourish peripheral tissue but only fructose cannot penetrate the blood-brain barrier. Also, 2-DG-induced feeding was abolished by i.v. infusion of .beta.-hydroxybutyrate, a substrate that can be oxidized by brain and other tissues but not by the liver.