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|Title:||Small intestinal glucose exposure determines the magnitude of the incretin effect in health and type 2 diabetes|
|Citation:||Diabetes, 2014; 63(8):2668-2675|
|Publisher:||American Diabetes Association|
|Chinmay S. Marathe, Christopher K. Rayner, Michelle Bound, Helen Checklin, Scott Standfield, Judith Wishart, Kylie Lange, Karen L. Jones and Michael Horowitz|
|Abstract:||The potential influence of gastric emptying on the "incretin effect," mediated by glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), is unknown. The objectives of this study were to determine the effects of intraduodenal (ID) glucose infusions at 2 (ID2) and 4 (ID4) kcal/min (equating to two rates of gastric emptying within the physiological range) on the size of the incretin effect, gastrointestinal glucose disposal (GIGD), plasma GIP, GLP-1, and glucagon secretion in health and type 2 diabetes. We studied 10 male BMI-matched controls and 11 male type 2 patients managed by diet or metformin only. In both groups, GIP, GLP-1, and the magnitude of incretin effect were greater with ID4 than ID2, as was GIGD; plasma glucagon was suppressed by ID2, but not ID4. There was no difference in the incretin effect between the two groups. Based on these data, we conclude that the rate of small intestinal glucose exposure (i.e., glucose load) is a major determinant of the comparative secretion of GIP and GLP-1, as well as the magnitude of the incretin effect and GIGD in health and type 2 diabetes.|
|Keywords:||Diabetes Mellitus, Type 2; Gastric Inhibitory Polypeptide; Glucagon; Insulin; C-Peptide; Case-Control Studies; Gene Expression Regulation|
|Rights:||© 2014 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered|
|Appears in Collections:||Medicine publications|
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