Effect of chronic hyperghrelinemia on ingestive action of ghrelin

Wei Wei, Xiang Qi, Jason Reed, Jeff Ceci, Hui Qun Wang, Guiyun Wang, Ella W. Englander, George H. Greeley

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)R803-R808
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume290
Issue number3
DOIs
StatePublished - Mar 1 2006

Keywords

  • Fat pad
  • Food intake
  • Growth
  • Transgenic mice

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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