Capsaicin abolishes lipoprivic but not glucoprivic feeding in rats.

To assess the contribution of visceral sensory neurons to feeding induced by blockade of glucose and fatty acid metabolism, adult rats were anesthetized and treated systemically with capsaicin, a toxin that destroys fine-diameter unmyelinated primary sensory neurons, including many visceral sensory neurons. Rats were maintained on a fat-supplemented diet throughout experimentation. For feeding tests, intake of this diet was measured hourly for 6 h after systemic blockade of fatty acid or glucose utilization with mercaptoacetate (MA) or 2-deoxy-D-glucose (2-DG), respectively, after simultaneous administration of MA and 2-DG and after saline injection. 2-DG stimulated a dose-related feeding response that was similar in magnitude in both capsaicin and vehicle-treated rats. MA also stimulated a dose-related feeding response in vehicle-treated rats. However, capsaicin-treated rats did not eat in response to MA. In addition, 2-DG and MA were additive in their stimulation of feeding in vehicle-treated controls, but capsaicin-treated rats ate the same amount after 2-DG plus MA as they did in response to 2-DG alone. Thus glucoprivation and lipoprivation activate anatomically and chemically distinct receptors for the metabolic control of feeding.