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 journalArticle

66 Citations (Scopus)

Abstract

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
Volume72
Issue number1-2
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Neural Inhibition
Leptin
Stomach
Food
Meals
Paraventricular Hypothalamic Nucleus
Eating
Solitary Nucleus
Diet

Keywords

  • Nucleus of the solitary tract
  • Paraventricular nucleus
  • Satiety

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Physiology (medical)

Cite this

Leptin amplifies the feeding inhibition and neural activation arising from a gastric nutrient preload. / Emond, Michael; Ladenheim, Ellen E.; Schwartz, Gary J.; Moran, Timothy H.

In: Physiology and Behavior, Vol. 72, No. 1-2, 2001, p. 123-128.

Research output: Contribution to journalArticle

Emond, Michael ; Ladenheim, Ellen E. ; Schwartz, Gary J. ; Moran, Timothy H. / Leptin amplifies the feeding inhibition and neural activation arising from a gastric nutrient preload. In: Physiology and Behavior. 2001 ; Vol. 72, No. 1-2. pp. 123-128.
@article{10181bb66b0241c7a5835cc8a52a36a3,
title = "Leptin amplifies the feeding inhibition and neural activation arising from a gastric nutrient preload",
abstract = "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.",
keywords = "Nucleus of the solitary tract, Paraventricular nucleus, Satiety",
author = "Michael Emond and Ladenheim, {Ellen E.} and Schwartz, {Gary J.} and Moran, {Timothy H.}",
year = "2001",
doi = "10.1016/S0031-9384(00)00393-0",
language = "English (US)",
volume = "72",
pages = "123--128",
journal = "Physiology and Behavior",
issn = "0031-9384",
publisher = "Elsevier Inc.",
number = "1-2",

}

TY - JOUR

T1 - Leptin amplifies the feeding inhibition and neural activation arising from a gastric nutrient preload

AU - Emond, Michael

AU - Ladenheim, Ellen E.

AU - Schwartz, Gary J.

AU - Moran, Timothy H.

PY - 2001

Y1 - 2001

N2 - 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.

AB - 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.

KW - Nucleus of the solitary tract

KW - Paraventricular nucleus

KW - Satiety

UR - http://www.scopus.com/inward/record.url?scp=0035120192&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035120192&partnerID=8YFLogxK

U2 - 10.1016/S0031-9384(00)00393-0

DO - 10.1016/S0031-9384(00)00393-0

M3 - Article

C2 - 11239989

AN - SCOPUS:0035120192

VL - 72

SP - 123

EP - 128

JO - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

IS - 1-2

ER -