Feeding was induced with lateral intracerebroventricular (ICV) injections of 2-deoxy-D-glucose (2-dg), a glucose analogue causing glucoprivation. Feeding increased rapidly by an average of 2.6 g following ICV 2-DG (2.9 or 5.8 mg per rat), but did not increase after ICV D-glucose or sucrose. At the same doses, 2-DG did not increase feeding when given peripherally. Core temperature dropped in a dose-dependent manner with doses of 2-DG sufficient to induce feeding after peripheral administration, but did not occur with ICV injections. The 2-DG (0.006--1.219 M) did not stimulate feeding when infused bilaterally into the lateral hypothalamus, the preoptic area, or the anterior lateral hypothalamus. Nor did it produce feeding when injected into the ventromedial hypothalamus at the same sites and in the same rats in which procaine HC1 caused increased feeding. The brain, therefore, is directly sensitive to glucoprivation in the control of feeding, and glucoprivation alone is sufficient to mobilize feeding behavior. The specific site of sensitivity to glucoprivation and the mode of action of the glucoprivic system in the brain are unknown.
GABAergic function in the lateral hypothalamus regulates feeding behavior: Possible mediation via orexin
