Journal article
V. Kesherwani, Vishalakshi Chavali, Bryan T. Hackfort, S. Tyagi, P. Mishra
Frontiers in Physiology, 2015
Frontiers in Physiology, 2015
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APA
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Kesherwani, V., Chavali, V., Hackfort, B. T., Tyagi, S., & Mishra, P. (2015). Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10. Frontiers in Physiology.
Chicago/Turabian
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Kesherwani, V., Vishalakshi Chavali, Bryan T. Hackfort, S. Tyagi, and P. Mishra. “Exercise Ameliorates High Fat Diet Induced Cardiac Dysfunction by Increasing Interleukin 10.” Frontiers in Physiology (2015).
MLA
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Kesherwani, V., et al. “Exercise Ameliorates High Fat Diet Induced Cardiac Dysfunction by Increasing Interleukin 10.” Frontiers in Physiology, 2015.
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@article{v2015a,
title = {Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10},
year = {2015},
journal = {Frontiers in Physiology},
author = {Kesherwani, V. and Chavali, Vishalakshi and Hackfort, Bryan T. and Tyagi, S. and Mishra, P.}
}
Abstract
Increasing evidence suggests that a sedentary lifestyle and a high fat diet (HFD) leads to cardiomyopathy. Moderate exercise ameliorates cardiac dysfunction, however underlying molecular mechanisms are poorly understood. Increased inflammation due to induction of pro-inflammatory cytokine such as tumor necrosis factor-alpha (TNF-α) and attenuation of anti-inflammatory cytokine such as interleukin 10 (IL-10) contributes to cardiac dysfunction in obese and diabetics. We hypothesized that exercise training ameliorates HFD- induced cardiac dysfunction by mitigating obesity and inflammation through upregulation of IL-10 and downregulation of TNF-α. To test this hypothesis, 8 week old, female C57BL/6J mice were fed with HFD and exercised (swimming 1 h/day for 5 days/week for 8 weeks). The four treatment groups: normal diet (ND), HFD, HFD + exercise (HFD + Ex) and ND + Ex were analyzed for mean body weight, blood glucose level, TNF-α, IL-10, cardiac fibrosis by Masson Trichrome, and cardiac dysfunction by echocardiography. Mean body weights were increased in HFD but comparatively less in HFD + Ex. The level of TNF-α was elevated and IL-10 was downregulated in HFD but ameliorated in HFD + Ex. Cardiac fibrosis increased in HFD and was attenuated by exercise in the HFD + Ex group. The percentage ejection fraction and fractional shortening were decreased in HFD but comparatively increased in HFD + Ex. There was no difference between ND and ND + Ex for the above parameters except an increase in IL-10 level following exercise. Based on these results, we conclude that exercise mitigates HFD- induced cardiomyopathy by decreasing obesity, inducing IL-10, and reducing TNF-α in mice.
