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

Michael Emond, Ellen E. Ladenheim, Gary J. Schwartz, Timothy H. Moran

Research output: Contribution to journalArticlepeer-review

69 Scopus citations


Leptin affects food intake by reducing meal size, suggesting that it may modulate the efficacy of within-meal satiety signals. To assess whether leptin would amplify the feeding inhibitory actions of a nutrient gastric preload, we compared liquid diet food intake and patterns of c-Fos activation in response to intraventricular leptin (3.5 μg), intragastric Ensure (10 ml over 10 min), or their combination. Leptin alone did not affect Ensure intake but significantly increased the suppression of intake produced by the intragastric preload. Within the nucleus of the solitary tract (NTS), leptin alone did not stimulate c-Fos but significantly elevated the number of c-Fos positive cells in response to intragastric Ensure at medial and rostral levels. Within the paraventricular nucleus (PVN), both leptin and the gastric load stimulated c-Fos expression, but the combination resulted in significantly greater number of c-Fos positive cells. These data demonstrate that leptin modulates the feeding inhibition produced by meal-related signals and suggest that this modulation occurs at the levels of the NTS and PVN.

Original languageEnglish (US)
Pages (from-to)123-128
Number of pages6
JournalPhysiology and Behavior
Issue number1-2
StatePublished - 2001
Externally publishedYes


  • Nucleus of the solitary tract
  • Paraventricular nucleus
  • Satiety

ASJC Scopus subject areas

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience


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