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Am J Physiol Regul Integr Comp Physiol (October 6, 2005). doi:10.1152/ajpregu.00331.2005
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Submitted on May 9, 2005
Accepted on September 30, 2005

EFFECT OF CHRONIC HYPERGHRELINEMIA ON INGESTIVE ACTION OF GHRELIN

Wei Wei1, Xiang Qi1, Jason Reed1, Jeff Ceci2, Hui-Qun Wang2, Guiyun Wang1, Ella W Englander1, and George H Greeley, Jr.1*

1 Department of Surgery, University of Texas Medical Branch, Galveston, Texas, USA
2 Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas, USA

* To whom correspondence should be addressed. E-mail: ggreeley{at}utmb.edu.

The stomach hormone, ghrelin, is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Systemic administration of ghrelin will cause elevations in GH secretion, food intake, adiposity and body growth. Ghrelin also affects insulin secretion, gastric acid secretion and gastric motility. Several reports indicate that repeated or continuous activation of GHS-R by exogenous GHSs or ghrelin results in a diminished GH secretory response. The purpose of this study was to examine the extent to which the acute stimulation of food intake by exogenous ghrelin is altered by chronic hyperghrelinemia in transgenic mice that over-express the human ghrelin gene. The present findings show that the orexigenic action of exogenous ghrelin is not diminished by a chronic hyperghrelinemia and indicate that the food ingestive pathway of the GHS-R is not susceptible to desensitization. In contrast, the epididymal fat pad growth response, like the GH response, to exogenous ghrelin is blunted in ghrelin transgenic mice with chronic hyperghrelinemia.




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