Incretins and islet function


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Abstract

Purpose of reviewTo examine the potential of incretin hormones, glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide, for the treatment of type 2 diabetes, with emphasis on glucagon-like peptide 1 receptor agonists and inhibitors of the enzyme dipeptidyl peptidase IV.Recent findingsGlucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide are released from the gut after meal ingestion; the release of glucagon-like peptide 1 is slightly impaired in individuals with type 2 diabetes. Both incretin hormones stimulate insulin secretion in a glucose-dependent manner and inhibit apoptosis in β cells, and glucagon-like peptide 1 inhibits glucagon secretion. Both incretins are rapidly inactivated by dipeptidyl peptidase IV. The enzyme inactivates the two incretins by removing their two N-terminal amino acids. This process is rapid, resulting in short circulating half-lives of the incretins. The combined action of glucagon-like peptide 1 to stimulate insulin secretion and inhibit glucagon secretion has formed the basis for the development of type 2 diabetes treatment. Two strategies of glucagon-like peptide 1-based therapy have been successful: one strategy uses dipeptidyl peptidase IV-resistant glucagon-like peptide 1 mimetics, whereas the other uses the inhibition of dipeptidyl peptidase IV. Both work in patients with type 2 diabetes, resulting in improved metabolic control.SummaryGlucagon-like peptide 1 receptor agonists and dipeptidyl peptidase IV inhibitors are beneficial in type 2 diabetes, which shows that an endogenous physiological pathway may be successful in treating one of the current major diseases.

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