TY - JOUR
T1 - High Methionine Diet Poses Cardiac Threat
T2 - A Molecular Insight
AU - Chaturvedi, Pankaj
AU - Kamat, Pradip K.
AU - Kalani, Anuradha
AU - Familtseva, Anastasia
AU - Tyagi, Suresh C.
N1 - Funding Information:
The work was partially supported by NIH grants HL-74185, HL-108621 and AHA grant 15POST23110021.
Publisher Copyright:
© 2015 Wiley Periodicals, Inc.
PY - 2016/7/1
Y1 - 2016/7/1
N2 - 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.
AB - 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.
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U2 - 10.1002/jcp.25247
DO - 10.1002/jcp.25247
M3 - Article
C2 - 26565991
AN - SCOPUS:84958206423
SN - 0021-9541
VL - 231
SP - 1554
EP - 1561
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
IS - 7
ER -