Circulating Levels of Ghrelin and GLP-1 are Inversely Related During Glucose Ingestion

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Abstract
Appetite regulation, and in particular the hypothalamic appetite-regulating network, has gained increasing interest during the past years due to the gross impact of obesity on human disease. The recent discovery of the endogenous ligand for the growth hormone secretagogue receptor (GHS-R) ghrelin [ 1 ] [ 2 ], which plays a role in reducing fat utilization and increasing body weight has been of special interest [ 3 ] [ 4 ]. When injected specifically into appetite-regulating hypothalamic nuclei in rats, hyperphagia is induced [ 5 ] [ 6 ]. Finally, ghrelin has been demonstrated to enhance gastric motility in rodents [ 7 ]. In contrast to the orexigenic actions of ghrelin, another peptide released from the gastrointestinal tract, glucagon-like peptide 1 (GLP-1), induces satiety [ 8 ] [ 9 ] [ 10 ]. Whereas a possible direct impact of ghrelin on the metabolism remains to be defined, several studies such as Ørskov et al. [ 11 ] have failed to demonstrate a direct effect of GLP-1 on insulin-stimulated glucose metabolism. Whether GLP-1 per se influences lipid metabolism remains subject to controversy [ 12 ] [ 13 ]. Since ghrelin and GLP-1 appear to have opposite effects on satiety and gastrointestinal motility, we carried out the present study to explore the impact of a classic caloric challenge - an oral glucose tolerance test (OGTT) - on the dynamics of circulating ghrelin and GLP-1 levels.

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