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Am J Physiol Regul Integr Comp Physiol 290: R803-R808, 2006. First published October 6, 2005; doi:10.1152/ajpregu.00331.2005
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Effect of chronic hyperghrelinemia on ingestive action of ghrelin

Wei Wei,1 Xiang Qi,1 Jason Reed,1 Jeff Ceci,2 Hui-Qun Wang,2 Guiyun Wang,1 Ella W. Englander,1 and George H. Greeley, Jr.1

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

Submitted 9 May 2005 ; accepted in final form 30 September 2005

The stomach hormone ghrelin is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Systemic administration of ghrelin will cause elevations in growth hormone (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 overexpress 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.

food intake; transgenic mice; growth; fat pad



Address for reprint requests and other correspondence: G. H. Greeley, Jr., Dept. of Surgery, The Univ. of Texas Medical Branch, 301 Univ. Boulevard, Galveston, TX 77555-0725 (e-mail: ggreeley{at}utmb.edu)




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