Exercise training reduces insulin resistance in postmyocardial infarction rats

Exercise training reduces insulin resistance in postmyocardial infarction rats

Myocardial infarction (MI) induces cardiac dysfunction and insulin resistance (IR). This study examines the effects of MI-related IR on vasorelaxation and its underlying mechanisms, with a specific focus on the role of exercise in reversing the impaired vasorelaxation. Adult male Sprague–Dawley rats...

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Main Authors: Wang, Youhua, Tian, Zhenjun, Zang, Weijin, Jiang, Hongke, Li, Youyou, Wang, Shengpeng, Chen, Shengfeng
Format: Online
Language:English
Published: BlackWell Publishing Ltd 2015
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425954/
id pubmed-4425954
recordtype oai_dc
spelling pubmed-44259542015-05-14 Exercise training reduces insulin resistance in postmyocardial infarction rats Wang, Youhua Tian, Zhenjun Zang, Weijin Jiang, Hongke Li, Youyou Wang, Shengpeng Chen, Shengfeng Original Research Myocardial infarction (MI) induces cardiac dysfunction and insulin resistance (IR). This study examines the effects of MI-related IR on vasorelaxation and its underlying mechanisms, with a specific focus on the role of exercise in reversing the impaired vasorelaxation. Adult male Sprague–Dawley rats were divided into three groups: Sham, MI, and MI+Exercise. MI+Exercise rats were subjected to 8 weeks of treadmill training. Cardiac contraction, myocardial and arterial structure, vasorelaxation, levels of inflammatory cytokines, expression of eNOS and TNF-α, and activation of PI3K/Akt/eNOS and p38 mitogen-activated protein kinase (p38 MAPK) were determined in aortas. MI significantly impaired endothelial structure and vasodilation (P < 0.05–0.01), as indicated by decreased arterial vasorelaxation to ACh and insulin. MI also attenuated the myocardial contractile response, decreased aortic PI3K/Akt/eNOS expression and phosphorylation by insulin, and increased IL-1β, IL-6, and TNF-α expression and p38 MAPK activity (P < 0.05–0.01). Exercise improved insulin sensitivity in aortas, facilitated myocardial contractile response and arterial vasorelaxation to ACh and insulin, and increased arterial PI3K/Akt/eNOS activity. Moreover, exercise markedly reversed increased p38 MAPK activity and normalized inflammatory cytokines in post-MI arteries. Inhibition of PI3K with LY-294002, and eNOS with L-NAME significantly blocked arterial vasorelaxation and PI3K/Akt/eNOS phosphorylation in response to insulin. In conclusion, these results demonstrate that endothelial dysfunction in response to insulin plays an important role in MI-related IR. The reversal of IR by exercise is most likely associated with normalizing inflammatory cytokines, increasing the activation of PI3K/Akt/eNOS, and reducing the activation of p38 MAPK. BlackWell Publishing Ltd 2015-04-23 /pmc/articles/PMC4425954/ /pubmed/25907785 http://dx.doi.org/10.14814/phy2.12339 Text en © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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 Wang, Youhua
Tian, Zhenjun
Zang, Weijin
Jiang, Hongke
Li, Youyou
Wang, Shengpeng
Chen, Shengfeng
spellingShingle Wang, Youhua
Tian, Zhenjun
Zang, Weijin
Jiang, Hongke
Li, Youyou
Wang, Shengpeng
Chen, Shengfeng
Exercise training reduces insulin resistance in postmyocardial infarction rats
author_facet Wang, Youhua
Tian, Zhenjun
Zang, Weijin
Jiang, Hongke
Li, Youyou
Wang, Shengpeng
Chen, Shengfeng
author_sort Wang, Youhua
title Exercise training reduces insulin resistance in postmyocardial infarction rats
title_short Exercise training reduces insulin resistance in postmyocardial infarction rats
title_full Exercise training reduces insulin resistance in postmyocardial infarction rats
title_fullStr Exercise training reduces insulin resistance in postmyocardial infarction rats
title_full_unstemmed Exercise training reduces insulin resistance in postmyocardial infarction rats
title_sort exercise training reduces insulin resistance in postmyocardial infarction rats
description Myocardial infarction (MI) induces cardiac dysfunction and insulin resistance (IR). This study examines the effects of MI-related IR on vasorelaxation and its underlying mechanisms, with a specific focus on the role of exercise in reversing the impaired vasorelaxation. Adult male Sprague–Dawley rats were divided into three groups: Sham, MI, and MI+Exercise. MI+Exercise rats were subjected to 8 weeks of treadmill training. Cardiac contraction, myocardial and arterial structure, vasorelaxation, levels of inflammatory cytokines, expression of eNOS and TNF-α, and activation of PI3K/Akt/eNOS and p38 mitogen-activated protein kinase (p38 MAPK) were determined in aortas. MI significantly impaired endothelial structure and vasodilation (P < 0.05–0.01), as indicated by decreased arterial vasorelaxation to ACh and insulin. MI also attenuated the myocardial contractile response, decreased aortic PI3K/Akt/eNOS expression and phosphorylation by insulin, and increased IL-1β, IL-6, and TNF-α expression and p38 MAPK activity (P < 0.05–0.01). Exercise improved insulin sensitivity in aortas, facilitated myocardial contractile response and arterial vasorelaxation to ACh and insulin, and increased arterial PI3K/Akt/eNOS activity. Moreover, exercise markedly reversed increased p38 MAPK activity and normalized inflammatory cytokines in post-MI arteries. Inhibition of PI3K with LY-294002, and eNOS with L-NAME significantly blocked arterial vasorelaxation and PI3K/Akt/eNOS phosphorylation in response to insulin. In conclusion, these results demonstrate that endothelial dysfunction in response to insulin plays an important role in MI-related IR. The reversal of IR by exercise is most likely associated with normalizing inflammatory cytokines, increasing the activation of PI3K/Akt/eNOS, and reducing the activation of p38 MAPK.
publisher BlackWell Publishing Ltd
publishDate 2015
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425954/
_version_ 1613221449139486720

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