Ability of GLP-1 to decrease food intake is dependent on nutritional status

Charlotte C. Ronveaux, Guillaume de Lartigue, Helen E Raybould

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Gut-derived glucagon like peptide-1 (GLP-1) acts in the postprandial period to stimulate insulin secretion and inhibit gastrointestinal motor and secretory function; whether endogenous peripheral GLP-1 inhibits food intake is less clear. We hypothesized that GLP-1 inhibits food intake in the fed, but not fasted, state. There is evidence that GLP-1 acts via stimulation of vagal afferent neurons (VAN); we further hypothesized that the satiating effects of endogenous GLP-1 in the postprandial period is determined either by a change in GLP-1 receptor (GLP-1R) expression or localization to different cellular compartments in VAN. Methods: Food intake was recorded following administration of GLP-1 (50. μg/kg or 100. μg/kg) or saline (IP) in Wistar rats fasted for 18. h or fasted then re-fed with 3. g chow. GLP-1R protein expression and localization on VAN were determined by immunocytochemistry and immunoblots in animals fasted for 18. h or fasted then re-fed for 40. min. GLP-1R mRNA level was detected in animals fasted for 18. h or fasted and re-fed ad libitum for 2. h. Results: GLP-1 (100. μg/kg) significantly reduced 40. min food intake by 38% in re-fed but not fasted rats (p. <. 0.05). GLP-1R mRNA or protein levels in VAN were unchanged in re-fed compared to fasted rats. However, GLP-1R localization to the plasma membrane was significantly increased in VAN by feeding. Conclusion: Feeding changes the ability of peripheral GLP-1 to inhibit food intake. GLP-1Rs are trafficked to the plasma membrane in response to a meal. GLP-1 may play a role in regulating food intake in the postprandial period.

Original languageEnglish (US)
Pages (from-to)222-229
Number of pages8
JournalPhysiology and Behavior
Volume135
DOIs
StatePublished - 2014

Fingerprint

Glucagon-Like Peptide 1
Nutritional Status
Eating
Afferent Neurons
Postprandial Period
Cell Membrane
Glucagon-Like Peptides
Intake
Food
Messenger RNA
Neuron
Meals
Wistar Rats
Proteins
Immunohistochemistry
Glucagon-Like Peptide-1 Receptor
Insulin
Localization
Rat

Keywords

  • Food intake
  • Glucagon-like-peptide-1
  • Receptor trafficking
  • Vagal afferent neurons

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Experimental and Cognitive Psychology
  • Philosophy

Cite this

Ability of GLP-1 to decrease food intake is dependent on nutritional status. / Ronveaux, Charlotte C.; de Lartigue, Guillaume; Raybould, Helen E.

In: Physiology and Behavior, Vol. 135, 2014, p. 222-229.

Research output: Contribution to journalArticle

Ronveaux, Charlotte C. ; de Lartigue, Guillaume ; Raybould, Helen E. / Ability of GLP-1 to decrease food intake is dependent on nutritional status. In: Physiology and Behavior. 2014 ; Vol. 135. pp. 222-229.
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abstract = "Gut-derived glucagon like peptide-1 (GLP-1) acts in the postprandial period to stimulate insulin secretion and inhibit gastrointestinal motor and secretory function; whether endogenous peripheral GLP-1 inhibits food intake is less clear. We hypothesized that GLP-1 inhibits food intake in the fed, but not fasted, state. There is evidence that GLP-1 acts via stimulation of vagal afferent neurons (VAN); we further hypothesized that the satiating effects of endogenous GLP-1 in the postprandial period is determined either by a change in GLP-1 receptor (GLP-1R) expression or localization to different cellular compartments in VAN. Methods: Food intake was recorded following administration of GLP-1 (50. μg/kg or 100. μg/kg) or saline (IP) in Wistar rats fasted for 18. h or fasted then re-fed with 3. g chow. GLP-1R protein expression and localization on VAN were determined by immunocytochemistry and immunoblots in animals fasted for 18. h or fasted then re-fed for 40. min. GLP-1R mRNA level was detected in animals fasted for 18. h or fasted and re-fed ad libitum for 2. h. Results: GLP-1 (100. μg/kg) significantly reduced 40. min food intake by 38{\%} in re-fed but not fasted rats (p. <. 0.05). GLP-1R mRNA or protein levels in VAN were unchanged in re-fed compared to fasted rats. However, GLP-1R localization to the plasma membrane was significantly increased in VAN by feeding. Conclusion: Feeding changes the ability of peripheral GLP-1 to inhibit food intake. GLP-1Rs are trafficked to the plasma membrane in response to a meal. GLP-1 may play a role in regulating food intake in the postprandial period.",
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AB - Gut-derived glucagon like peptide-1 (GLP-1) acts in the postprandial period to stimulate insulin secretion and inhibit gastrointestinal motor and secretory function; whether endogenous peripheral GLP-1 inhibits food intake is less clear. We hypothesized that GLP-1 inhibits food intake in the fed, but not fasted, state. There is evidence that GLP-1 acts via stimulation of vagal afferent neurons (VAN); we further hypothesized that the satiating effects of endogenous GLP-1 in the postprandial period is determined either by a change in GLP-1 receptor (GLP-1R) expression or localization to different cellular compartments in VAN. Methods: Food intake was recorded following administration of GLP-1 (50. μg/kg or 100. μg/kg) or saline (IP) in Wistar rats fasted for 18. h or fasted then re-fed with 3. g chow. GLP-1R protein expression and localization on VAN were determined by immunocytochemistry and immunoblots in animals fasted for 18. h or fasted then re-fed for 40. min. GLP-1R mRNA level was detected in animals fasted for 18. h or fasted and re-fed ad libitum for 2. h. Results: GLP-1 (100. μg/kg) significantly reduced 40. min food intake by 38% in re-fed but not fasted rats (p. <. 0.05). GLP-1R mRNA or protein levels in VAN were unchanged in re-fed compared to fasted rats. However, GLP-1R localization to the plasma membrane was significantly increased in VAN by feeding. Conclusion: Feeding changes the ability of peripheral GLP-1 to inhibit food intake. GLP-1Rs are trafficked to the plasma membrane in response to a meal. GLP-1 may play a role in regulating food intake in the postprandial period.

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