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Research Article Free access | 10.1172/JCI116186

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

M A Nauck, M M Heimesaat, C Orskov, J J Holst, R Ebert, and W Creutzfeldt

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

Find articles by Nauck, M. in: PubMed | Google Scholar

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

Find articles by Heimesaat, M. in: PubMed | Google Scholar

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

Find articles by Orskov, C. in: PubMed | Google Scholar

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

Find articles by Holst, J. in: PubMed | Google Scholar

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

Find articles by Ebert, R. in: PubMed | Google Scholar

Department of Medicine, Georg-August-Universität, Göttingen, Federal Republic of Germany.

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Published January 1, 1993 - More info

Published in Volume 91, Issue 1 on January 1, 1993
J Clin Invest. 1993;91(1):301–307. https://doi.org/10.1172/JCI116186.
© 1993 The American Society for Clinical Investigation
Published January 1, 1993 - Version history
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Abstract

In type-2 diabetes, the overall incretin effect is reduced. The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). With GIP, the maximum effect in type-2 diabetic patients was significantly lower (by 54%; P < 0.05) than in normal subjects. With GLP-1 [7-36 amide] type-2 diabetic patients reached 71% of the increments in C-peptide of normal subjects (difference not significant). Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. It also lowers glucagon concentrations.

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