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Structure and Function of the Glucagon-Like Peptide-1 Receptor

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Glucagon III

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 123))

Abstract

The postprandial increase in plasma insulin level is the result not only of a rise in blood glucose concentration but of a combined effect of glucose and hormones secreted by gut endocrine cells (Ebert and Creutzfeld 1987; Dupre 1991). The contribution of intestinal factors in the stimulation of pancreatic endocrine secretions has been recognized for a long time. At the beginning of this century studies suggested that gut “secretins” were able to stimulate pancreatic endocrine and exocrine secretions (Moore et al. 1906). The identification of neuronal and hormonal factors originating from the intestine which control either positively or negatively the function of the endocrine pancreas led to the notion of an entero-insular axis (Unger and Eisentraut 1969). With the development of peptide chemistry and the more recent progress in the molecular biological characterization of hormone genes, the most important factors involved in the stimulation of glucose-induced insulin secretion have now been identified. These are GIP (glucose-dependent insulinotropic polypeptide or gastric inhibitory polypeptide) and GLP-1 (glucagon-like peptide-1).

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Thorens, B., Widmann, C. (1996). Structure and Function of the Glucagon-Like Peptide-1 Receptor. In: Lefèbvre, P.J. (eds) Glucagon III. Handbook of Experimental Pharmacology, vol 123. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-61150-6_16

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