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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2002-12, Vol.283 (6), p.1321-R1326
Hauptverfasser: Richardson, Ralph D, Omachi, Koichi, Kermani, Rasoul, Woods, Stephen C
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
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.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00521.2001