Abstract
To evaluate the role of visceral vagal afferent fibers and glucocorticoid in lipopolysaccaride (LPS)-induced feed-suppression, we observed the food intake and body weight in intact or vagotomized rats starting 2 days before, and continuing 6 days after an administration of 100 μg/kg LPS via the intraperitoneal (ip) route with or without methylpredonisolone succinate (MPDN, artificial glucocorticoid). Vagotomy was performed by one of three ways: (a) selective vagotomy in hepatic (HVX), gastric (GVX), or celiac (CVX) branches; (b) combined vagotomy (HVX+CVX, CVX+GVX, or GVX+HVX); (c) total subdiaphragmatic vagotomy (TVX). Feed-suppression induced by LPS was attenuated in the following order of rats with HVX, GVX, and CVX. Attenuation of LPS-induced anorexia in rats with HVX+GVX was greater than that in any animals with the single or combined vagotomy. However, not only GVX+HVX but also TVX failed to restore the complete food intake impaired by LPS. The anorexia and weight-reducing evoked by LPS was prevented markedly in rats given 150 μg/kg MPDN into the third cerebral ventricle. When 150 μg/kg MPDN, however, was given via the ip route, such preventions were not observed. We conclude 1) that both afferent signals via the hepatic and gastric vagus branches play an important role in the feed-suppression induced by LPS, and 2) that another factors other than vagal afferent signal may be involved in the LPS-induced feed suppression. Furthermore, MPDN ameliorates the LPS-evoked anorexia within the central nervous system. [Jpn J Physiol 54 Suppl:S187 (2004)]
