Format

Send to

Choose Destination
See comment in PubMed Commons below
J Clin Endocrinol Metab. 2008 Nov;93(11 Suppl 1):S37-50. doi: 10.1210/jc.2008-1630.

Central control of body weight and appetite.

Author information

1
Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, USA. steve.woods@psychiatry.uc.edu

Abstract

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.

PMID:
18987269
PMCID:
PMC2585760
DOI:
10.1210/jc.2008-1630
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Silverchair Information Systems Icon for PubMed Central
    Loading ...
    Support Center