Insulin, cGMP, and TGF-β Signals Regulate Food Intake and Quiescence in C. elegans: A Model for Satiety

Young jai You, Jeongho Kim, David M. Raizen, Leon Avery

Research output: Contribution to journalArticlepeer-review

165 Scopus citations

Abstract

Despite the prevalence of obesity and its related diseases, the signaling pathways for appetite control and satiety are not clearly understood. Here we report C. elegans quiescence behavior, a cessation of food intake and movement that is possibly a result of satiety. C. elegans quiescence shares several characteristics of satiety in mammals. It is induced by high-quality food, it requires nutritional signals from the intestine, and it depends on prior feeding history: fasting enhances quiescence after refeeding. During refeeding after fasting, quiescence is evoked, causing gradual inhibition of food intake and movement, mimicking the behavioral sequence of satiety in mammals. Based on these similarities, we propose that quiescence results from satiety. This hypothesized satiety-induced quiescence is regulated by peptide signals such as insulin and TGF-β. The EGL-4 cGMP-dependent protein kinase functions downstream of insulin and TGF-β in sensory neurons including ASI to control quiescence in response to food intake.

Original languageEnglish (US)
Pages (from-to)249-257
Number of pages9
JournalCell Metabolism
Volume7
Issue number3
DOIs
StatePublished - Mar 5 2008

Keywords

  • HUMDISEASE
  • MOLNEURO

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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