Intraventricular insulin potentiates the anorexic effect of corticotropin releasing hormone in rats
1 Veterans Affairs Puget Sound Health Care System, Seattle 98108; 2 Department of Psychiatry and Behavioral Sciences and 3 School of Dentistry, University of Washington, Seattle, Washington 98195; 4 University of Tehran, Tehran, Iran; and 5 Department of Psychiatry, University of Cincinnati, Ci...
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Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2002-12, Vol.283 (6), p.1321-R1326 |
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Sprache: | eng |
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Zusammenfassung: | 1 Veterans Affairs Puget Sound Health Care System,
Seattle 98108; 2 Department of Psychiatry and
Behavioral Sciences and 3 School of Dentistry,
University of Washington, Seattle, Washington 98195;
4 University of Tehran, Tehran, Iran;
and 5 Department of Psychiatry, University of
Cincinnati, Cincinnati, Ohio 45267
Intraventricular
corticotropin releasing hormone (CRH) suppresses food intake and
body weight as a stress response. Insulin, acting within the brain,
also suppresses food intake and body weight, and this suppression is
related to caloric homeostasis. We determined if increased insulin
within the brain potentiates the anorexic effects of intraventricular
CRH. Rats were food deprived for 17 h each day and then given
30-min access to Ensure. One-half received continuous third ventricular
infusion of synthetic cerebrospinal fluid via osmotic minipumps, and
one-half received insulin (0.6 mU/day). During the infusion, rats also
received 0, 0.1, 1.0, or 5.0 µg of CRH into the lateral ventricle
just before access to Ensure. Insulin alone had no effect on Ensure
intake or body weight. CRH dose dependently reduced Ensure intake in
both groups, and the reduction was greater in the insulin group. Hence,
central insulin potentiated the ability of centrally administered CRH to suppress food intake. These findings suggest that stress-related influences over food intake, particularly those mediated via CRH, interact with relative adiposity as signaled to the brain by central insulin.
food intake; body weight; obesity; satiety
Deceased 1998. |
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ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.00521.2001 |