Central control of body weight and appetite.

Journal Article (Journal Article;Review)

CONTEXT: Energy balance is critical for survival and health, and control of food intake is an integral part of this process. This report reviews hormonal signals that influence food intake and their clinical applications. EVIDENCE ACQUISITION: A relatively novel insight is that satiation signals that control meal size and adiposity signals that signify the amount of body fat are distinct and interact in the hypothalamus and elsewhere to control energy homeostasis. This review focuses upon recent literature addressing the integration of satiation and adiposity signals and therapeutic implications for treatment of obesity. EVIDENCE SYNTHESIS: During meals, signals such as cholecystokinin arise primarily from the GI tract to cause satiation and meal termination; signals secreted in proportion to body fat such as insulin and leptin interact with satiation signals and provide effective regulation by dictating meal size to amounts that are appropriate for body fatness, or stored energy. Although satiation and adiposity signals are myriad and redundant and reduce food intake, there are few known orexigenic signals; thus, initiation of meals is not subject to the degree of homeostatic regulation that cessation of eating is. There are now drugs available that act through receptors for satiation factors and which cause weight loss, demonstrating that this system is amenable to manipulation for therapeutic goals. CONCLUSIONS: Although progress on effective medical therapies for obesity has been relatively slow in coming, advances in understanding the central regulation of food intake may ultimately be turned into useful treatment options.

Full Text

Duke Authors

Cited Authors

  • Woods, SC; D'Alessio, DA

Published Date

  • November 2008

Published In

Volume / Issue

  • 93 / 11 Suppl 1

Start / End Page

  • S37 - S50

PubMed ID

  • 18987269

Pubmed Central ID

  • PMC2585760

International Standard Serial Number (ISSN)

  • 0021-972X

Digital Object Identifier (DOI)

  • 10.1210/jc.2008-1630


  • eng

Conference Location

  • United States