Incretin hormones as immunomodulators of atherosclerosis

Atherosclerosis results from endothelial cell dysfunction and inflammatory processes affecting both macro- and microvasculature which are involved in vascular diabetic complications. Glucagon-like peptide-1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrie...

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Main Authors: Alonso, Nuria, Julián, M. Teresa, Puig-Domingo, Manuel, Vives-Pi, Marta
Format: Online
Language:English
Published: Frontiers Research Foundation 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435665/
id pubmed-3435665
recordtype oai_dc
spelling pubmed-34356652012-09-12 Incretin hormones as immunomodulators of atherosclerosis Alonso, Nuria Julián, M. Teresa Puig-Domingo, Manuel Vives-Pi, Marta Endocrinology Atherosclerosis results from endothelial cell dysfunction and inflammatory processes affecting both macro- and microvasculature which are involved in vascular diabetic complications. Glucagon-like peptide-1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally as opposed to intravenously and it retains its insulinotropic activity in patients with type 2 diabetes mellitus (T2D). GLP-1 based therapies, such as GLP-1 receptor (GLP-1R) agonists and inhibitors of dipeptidyl peptidase-4, an enzyme that degrades endogenous GLP-1 are routinely used to treat patients with T2D. Recent experimental model studies have established that GLP-1R mRNA is widely expressed in several immune cells. Moreover, its activation contributes to the regulation of both thymocyte and peripheral T cells proliferation and is involved in the maintenance of peripheral regulatory T cells. GLP-1R is also expressed in endothelial and smooth muscle cells. The effect of incretin hormones on atherosclerogenesis have recently been studied in animal models of apolipoprotein E-deficient mice (apoE-/-). These studies have demonstrated that treatment with incretin hormones or related compounds suppresses the progression of atherosclerosis and macrophage infiltration in the arterial wall as well as a marked anti-oxidative and anti-inflammatory effect on endothelial cells. This effect may have a major impact on the attenuation of atherosclerosis and may help in the design of new therapies for cardiovascular disease in patients with type 2 diabetes. Frontiers Research Foundation 2012-09-07 /pmc/articles/PMC3435665/ /pubmed/22973260 http://dx.doi.org/10.3389/fendo.2012.00112 Text en Copyright © Alonso, Julián, Puig-Domingo and Vives-Pi. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) , which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Alonso, Nuria
Julián, M. Teresa
Puig-Domingo, Manuel
Vives-Pi, Marta
spellingShingle Alonso, Nuria
Julián, M. Teresa
Puig-Domingo, Manuel
Vives-Pi, Marta
Incretin hormones as immunomodulators of atherosclerosis
author_facet Alonso, Nuria
Julián, M. Teresa
Puig-Domingo, Manuel
Vives-Pi, Marta
author_sort Alonso, Nuria
title Incretin hormones as immunomodulators of atherosclerosis
title_short Incretin hormones as immunomodulators of atherosclerosis
title_full Incretin hormones as immunomodulators of atherosclerosis
title_fullStr Incretin hormones as immunomodulators of atherosclerosis
title_full_unstemmed Incretin hormones as immunomodulators of atherosclerosis
title_sort incretin hormones as immunomodulators of atherosclerosis
description Atherosclerosis results from endothelial cell dysfunction and inflammatory processes affecting both macro- and microvasculature which are involved in vascular diabetic complications. Glucagon-like peptide-1 (GLP-1) is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally as opposed to intravenously and it retains its insulinotropic activity in patients with type 2 diabetes mellitus (T2D). GLP-1 based therapies, such as GLP-1 receptor (GLP-1R) agonists and inhibitors of dipeptidyl peptidase-4, an enzyme that degrades endogenous GLP-1 are routinely used to treat patients with T2D. Recent experimental model studies have established that GLP-1R mRNA is widely expressed in several immune cells. Moreover, its activation contributes to the regulation of both thymocyte and peripheral T cells proliferation and is involved in the maintenance of peripheral regulatory T cells. GLP-1R is also expressed in endothelial and smooth muscle cells. The effect of incretin hormones on atherosclerogenesis have recently been studied in animal models of apolipoprotein E-deficient mice (apoE-/-). These studies have demonstrated that treatment with incretin hormones or related compounds suppresses the progression of atherosclerosis and macrophage infiltration in the arterial wall as well as a marked anti-oxidative and anti-inflammatory effect on endothelial cells. This effect may have a major impact on the attenuation of atherosclerosis and may help in the design of new therapies for cardiovascular disease in patients with type 2 diabetes.
publisher Frontiers Research Foundation
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435665/
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