Leptin amplifies the feeding inhibition and neural activation arising froma gastric nutrient preload

Leptin affects food intake by reducing meal size, suggesting that it may mo dulate the efficacy of within-meal satiety signals. To assess whether lepti n would amplify the feeding inhibitory actions of a nutrient gastric preloa d, we compared liquid diet food intake and patterns of c-Fos activation in response to intraventricular leptin (3.5 mug), intragastric Ensure (10 mi o ver 10 min), or their combination. Leptin alone did not affect Ensure intak e but significantly increased the suppression of intake produced by the int ragastric preload. Within the nucleus of the solitary tract (NTS), leptin a lone did not stimulate c-Fos but significantly elevated the number of c-Fos positive cells in response to intragastric Ensure at medial and rostral le vels. Within the paraventricular nucleus (PVN), both leptin and the gastric load stimulated c-Fos expression, but the combination resulted in signific antly greater number of c-Fos positive cells. These data demonstrate that l eptin modulates the feeding inhibition produced by meal-related signals and suggest that this modulation occurs at the levels of the NTS and PVN.;(C) 2001 Elsevier Science Inc. All rights reserved.