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Abstract
Incretin hormones are defined as intestinal hormones released in response to nutrient
ingestion, which potentiate the glucose-induced insulin response. In humans, the incretin
effect is mainly caused by two peptide hormones, glucose-dependent insulin releasing
polypeptide GIP, and glucagon-like peptide-1 GLP-1. GIP is secreted by K cells from
the upper small intestine while GLP-1 is mainly produced in the enteroendocrine L
cells located in the distal intestine. Their effect is mediated through their binding
with specific receptors, though part of their biological action may also involve neural
modulation. GIP and GLP-1 are both rapidly degraded into inactive metabolites by the
enzyme dipeptidyl-peptidase-IV (DPP-IV). In addition to its effects on insulin secretion,
GLP-1 exerts other significant actions, including stimulation of insulin biosynthesis,
inhibition of glucagon secretion, inhibition of gastric emptying and acid secretion,
reduction of food intake, and trophic effects on the pancreas. As the insulinotropic
action of GLP-1 is preserved in type 2 diabetic patients, this peptide was a candidate
as a therapeutic agent for this disease. A number of pharmacological strategies have
been developed to provide continuous delivery of GLP-1 and to prevent degradation
of GLP-1, including continuous administration of GLP-1, DPP-IV inhibitors and DPP-IV
resistant GLP-1 analogues. Recent results of the most clinically advanced incretin
mimetics confirmed their efficacy to improve glycemic control in type 2 diabetic patients.
Further results are expected to confirm the efficacy/safety profile of these compounds,
and to find their place in the therapeutic strategy of type 2 diabetes.