Physiological satiety implications of gastrointestinal antiobesity surgery.


Journal Article

This manuscript reviews the known satiety signals and the impact of antiobesity surgery on these physiological satiety mechanisms. Satiety signals originate from the stomach and small bowel to stop eating behavior. Stomach signals (gastric distension) produce early satiety by releasing hypothalamic cholecystokinin (CCK). The intermeal interval is probably mediated by peripheral CCK released by a threshold level of intraluminal calories. Anti-obesity operations probably rely little on these physiological satiety signals. Gastric balloons and gastroplasty produce nonphysiological gastric distension whereas intestinal bypass causes malabsorption. Gastric bypass combines supramaximal gastric distension with taste aversion from dumping. Future physiological manipulation of the satiety cascade will lead to improve obesity intervention.

Full Text

Cited Authors

  • Pappas, TN

Published Date

  • February 1, 1992

Published In

Volume / Issue

  • 55 / 2 Suppl

Start / End Page

  • 571S - 572S

PubMed ID

  • 1733129

Pubmed Central ID

  • 1733129

International Standard Serial Number (ISSN)

  • 0002-9165

Digital Object Identifier (DOI)

  • 10.1093/ajcn/55.2.571s


  • eng

Conference Location

  • United States