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The GIuco-Incretin Hormone Glucagon-Like Peptide-1 and Its β-Cell Receptor

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Molecular Biology of Diabetes

Abstract

Glucose-induced insulin secretion can be stimulated or inhibited by a number of hormones or neurotransmitters. In particular, gut hormones have been suggested to have profound effects on the β-cells secretory activity. Indeed, it has been known for a long time that oral glucose ingestion induced a considerably greater elevation in plasma insulin levels compared to an intravenous glucose injection producing the same glycemia (1–3) and the existence of an “entero-insular axis,” which refers to the action of these putative intestinal hormones on the the endocrine pancreas, has been suggested (3). A number of peptides have been purified from intestinal extracts such as secretin, cholecystokinin (CCK), gastrin, gastrin releasing peptide, vasoactive intestinal polypeptide (VIP), or enteroglucagon (1–3), which were able to stimulate insulin secretion in the presence of normal or slightly elevated glucose concentrations. The “insulinotropic” or “gluco-incretin” activity of these peptides was, however, weak even at high pharmacological concentrations. Today, two principal gluco-incretins have been characterized: Gastric inhibitory peptide (GIP), also referred to as glucose-dependent insulinotropic polypeptide, and truncated forms of glucagon-like peptide 1, GLP- 1(7–37) or GLP-l(7–36)amide.

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Thorens, B. (1994). The GIuco-Incretin Hormone Glucagon-Like Peptide-1 and Its β-Cell Receptor. In: Draznin, B., LeRoith, D. (eds) Molecular Biology of Diabetes. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0241-7_15

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  • DOI: https://doi.org/10.1007/978-1-4612-0241-7_15

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