[HTML][HTML] GLP-1 effects on islets: hormonal, neuronal, or paracrine?

MY Donath, R Burcelin - Diabetes care, 2013 - ncbi.nlm.nih.gov
MY Donath, R Burcelin
Diabetes care, 2013ncbi.nlm.nih.gov
According to the classical incretin concept, glucagon-like peptide (GLP)-1 is viewed as a
hormone produced in the intestinal L cells and acting via the circulation on satiety in the
brain, gut motility, and insulin and glucagon secretion in the pancreatic islet. However, in
contrast to typical hormones, plasma levels of GLP-1 are relatively low with a very short half-
life. Furthermore, GLP-1 is rapidly inactivated by dipeptidyl peptidase-4 (DPP-4) in the
vicinity of L cells within, 1 min from the secretion of the gut peptide (1, 2). This rapid …
According to the classical incretin concept, glucagon-like peptide (GLP)-1 is viewed as a hormone produced in the intestinal L cells and acting via the circulation on satiety in the brain, gut motility, and insulin and glucagon secretion in the pancreatic islet. However, in contrast to typical hormones, plasma levels of GLP-1 are relatively low with a very short half-life. Furthermore, GLP-1 is rapidly inactivated by dipeptidyl peptidase-4 (DPP-4) in the vicinity of L cells within, 1 min from the secretion of the gut peptide (1, 2). This rapid metabolism of GLP-1 raises questions about how its effects are mediated on target organs such as pancreatic β-cells. In this review, we will discuss possible alternative pathways for the incretin effect on pancreatic islet. These involve L cell–derived GLP-1 via neuronal activation and α-cell–derived GLP-1 via auto/paracrine effects. Of note, GLP-1 is not acting alone, and its effect can be modulated by other factors including GIP. Since no data are available yet in the present context, we have limited this review to GLP-1.
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