Year-end Sale % OFF 
Abstract
The incretin hormone glucose‐dependent insulinotropic polypeptide (GIP) potentiates glucose‐stimulated insulin secretion, and affects β‐cell turnover. This study aimed at evaluating if some of the beneficial effects of GIP on glucose homeostasis can be explained by modulation of islet blood flow. Anesthetized Sprague–Dawley rats were infused intravenously with different doses of GIP (10, 20, or 60 ng/kg*min) for 30 min. Subsequent organ blood flow measurements were performed with microspheres. In separate animals, islets were perfused ex vivo with GIP (10−6–10−12 mol/L) during normo‐ and hyperglycemia and arteriolar responsiveness was recorded. The highest dose of GIP potentiated insulin secretion during hyperglycemia, but had no effect in normoglycemic rats. The highest GIP concentration decreased blood perfusion of whole pancreas, pancreatic islets, duodenum, colon, liver and kidneys. The decrease in blood flow was unaffected by ganglion blockade or adenosine receptor inhibition. In contrast to this, in single perfused islets GIP induced a dose‐dependent arteriolar dilation. Thus, high doses of GIP exert a direct dilatory effect on islet arterioles in isolated islets, but induce a generalized vasoconstriction in splanchnic organs, including the whole pancreas and islets, in vivo. The latter effect is unlikely to be mediated by adenosine, the autonomic nervous system, or endothelial mediators.
Highlights
Incretins are gut-derived hormones which potentiate glucose-stimulated insulin release after a meal (Drucker 2013)
The major incretins are glucagon-like peptide-1 (GLP-1), produced by L-cells, and glucose-dependent insulinotropic polypeptide (GIP), produced by K-cells
The main new findings in this study are that high, supraphysiological GIP concentrations decreased the blood flow in whole pancreas, pancreatic islets, duodenum, colon, liver, and kidneys thereby indicating a similar effect on blood flow in organs supplied by different arteries
Summary
Incretins are gut-derived hormones which potentiate glucose-stimulated insulin release after a meal (Drucker 2013). The major incretins are glucagon-like peptide-1 (GLP-1), produced by L-cells, and glucose-dependent insulinotropic polypeptide (GIP), produced by K-cells. Their effects follow hormone plasma concentrations and are fairly short-acting, since they are rapidly degraded by the ubiquitous exopeptidase dipeptidyl peptidase-4 4) and they are cleared by the kidneys (Holst and Gromada 2004) Both incretins act via specific receptors, which are present on b-cells, and numerous other cell types in the body. GLP-1 inhibits glucagon secretion, whereas GIP on the other hand stimulates glucagon secretion (Lyssenko et al 2011) Both incretins stimulate b-cell proliferation and inhibit b-cell apoptosis.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
