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High Methionine Diet Poses Cardiac Threat: A Molecular Insight
Author(s) -
Chaturvedi Pankaj,
Kamat Pradip K.,
Kalani Anuradha,
Familtseva Anastasia,
Tyagi Suresh C.
Publication year - 2016
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25247
Subject(s) - methionine , oxidative stress , medicine , cardiac function curve , downregulation and upregulation , endocrinology , homocysteine , ejection fraction , cystathionine beta synthase , chemistry , biology , biochemistry , heart failure , gene , amino acid
High methionine diet (HMD) for example red meat which includes lamb, beef, pork can pose cardiac threat and vascular dysfunction but the mechanisms are unclear. We hypothesize that a diet rich in methionine can malfunction the cardiovascular system in three ways: (1) by augmenting oxidative stress; (2) by inflammatory manifestations; and (3) by matrix/vascular remodeling. To test this hypothesis we used four groups of mice: (1) WT; (2) WT + methionine; (3) CBS +/− ; (4) CBS +/− +methionine. We observed high oxidative stress in mice fed with methionine which was even higher in CBS +/− and CBS +/− +methionine. Higher oxidative stress was indicated by high levels of SOD‐1 in methionine fed mouse hearts whereas IL‐1β, IL‐6, TNFα, and TLR4 showed high inflammatory manifestations. The upregulated levels of eNOS/iNOS and upregulated levels of MMP2/MMP9 along with high collagen deposition indicated vascular and matrix remodeling in methionine fed mouse. We evaluated the cardiac function which was dysregulated in the mice fed with HMD. These mice had decreased ejection fraction and left ventricular dysfunction which subsequently leads to adverse cardiac remodeling. In conclusion, our study clearly shows that HMD poses a cardiac threat by increasing oxidative stress, inflammatory manifestations, matrix/vascular remodeling, and decreased cardiac function. J. Cell. Physiol. 231: 1554–1561, 2016. © 2015 Wiley Periodicals, Inc.