title: High Methionine Diet Poses Cardiac Threat: A Molecular Insight.
abstract: 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.
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Pankaj
authors.initials: P
authors.lastname: Chaturvedi
authors.affiliation: Department of Anesthesiology, University of Florida, Gainesville, Florida.
authors.forename: Pradip K
authors.initials: PK
authors.lastname: Kamat
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Anuradha
authors.initials: A
authors.lastname: Kalani
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Anastasia
authors.initials: A
authors.lastname: Familtseva
authors.affiliation: Department of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
authors.forename: Suresh C
authors.initials: SC
authors.lastname: Tyagi
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004032:Diet / Q000009:adverse effects; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D008715:Methionine / Q000008:administration & dosage* / Q000009:adverse effects; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D014176:Protein Biosynthesis / Q000235:genetics; D000069466:Red Meat / Q000009:adverse effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D008715:Methionine