Paras Kumar Mishra, PhD

Associate Professor at University of Nebraska Medical Center


Curriculum vitae



Cellular and Integrative Physiology

University of Nebraska Medical Center



Exercise ameliorates high fat diet mediated inflammation, DNA methylation and heart failure in female mice


Journal article


Vishalakshi Chavali, Jessica M. Harris, S. Givvimani, Natia Qipshidze, Lawrence A Murphy, Geetansh Tyagi, Naira S. Metreveli, Suresh Tyagi, P. Mishra
2013

Semantic Scholar DOI
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APA   Click to copy
Chavali, V., Harris, J. M., Givvimani, S., Qipshidze, N., Murphy, L. A., Tyagi, G., … Mishra, P. (2013). Exercise ameliorates high fat diet mediated inflammation, DNA methylation and heart failure in female mice.


Chicago/Turabian   Click to copy
Chavali, Vishalakshi, Jessica M. Harris, S. Givvimani, Natia Qipshidze, Lawrence A Murphy, Geetansh Tyagi, Naira S. Metreveli, Suresh Tyagi, and P. Mishra. “Exercise Ameliorates High Fat Diet Mediated Inflammation, DNA Methylation and Heart Failure in Female Mice” (2013).


MLA   Click to copy
Chavali, Vishalakshi, et al. Exercise Ameliorates High Fat Diet Mediated Inflammation, DNA Methylation and Heart Failure in Female Mice. 2013.


BibTeX   Click to copy

@article{vishalakshi2013a,
  title = {Exercise ameliorates high fat diet mediated inflammation, DNA methylation and heart failure in female mice},
  year = {2013},
  author = {Chavali, Vishalakshi and Harris, Jessica M. and Givvimani, S. and Qipshidze, Natia and Murphy, Lawrence A and Tyagi, Geetansh and Metreveli, Naira S. and Tyagi, Suresh and Mishra, P.}
}

Abstract

High fat diet (HFD) causes obesity and T2D that increases the incidence of heart failure. Exercise mitigates obesity and T2D and ameliorates cardiomyopathy. However, the underlying mechanism is nebulous. We hypothesized that exercise ameliorates HFD mediated inflammation, DNA methylation and cardiac dysfunction in female mice. To test the hypothesis, twelve weeks C57BL/6J female mice were fed with normal (ND) and HFD, with and without swimming exercise for 8 weeks constituting four groups: (1) ND, (2) HFD, (3) ND and exercise (NDEx), and (4) HFD and exercise (HFDEx). The levels of anti‐inflammatory IL‐10 and DNA methyl transferase‐1, ‐3a (DNMT‐1 and ‐3a) were measured by RT‐QPCR, immunoblotting and immunohistochemistry. Cardiac dysfunction was assessed by M‐mode echocardiography. The results revealed that exercise induces IL‐10 and attenuates DNMT‐1 and ‐3a in HFD fed mice. The percentage ejection fraction (EF) and fractional shortening (FS) was decreased in HFD group but improved in HFDEx group (% EF: ND‐ 84.9±2.9, HFD‐54.9±4.3, HFDEx‐75.0±2.9, and NDEx‐93.5±1.9; % FS: ND‐ 52.9±2.6, HFD‐27.9±2.7, HFDEx‐42.5±2.9, and NDEx ‐ 65.9±3.7). These results suggest that exercise ameliorates HFD mediated cardiac dysfunction by suppressing inflammation and DNA methylation.


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