High-fat Diet Ameliorates Left Ventricular Remodeling and Dysfunction in a Mouse Model of Dilated Cardiomyopathy

Uri Amit 1,2 David Kain 1,2 Natalie Landa 1,2 Natali Molotski 1,2 Ariel Munitz 3 Micha Feinberg 1,2 Yariv Kanfi 4 Haim Cohen 4 Jonathan Leor 1,2
1Neufeld Cardiac Research Institute, Tel-Aviv University, Tel-Aviv
2Sheba Center for Regenerative Medicine, Stem Cell, and Tissue Engineering, Tel-Hashomer, Tel-Hashomer
3Department of Clinical Microbiology and Immunology, Tel-Aviv University, Tel-Aviv
4Mina & Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan

Background: Dietary fat intake affects the development and progression of heart failure. Recent studies in our lab have shown that Interleukin 13 receptor α1 (IL-13 Rα1) deficiency in mice leads to the development of dilated cardiomyopathy and left ventricular (LV) dysfunction. In this study we aimed to elucidate the role of high-fat diet on LV remodeling and dysfunction in Il13ra1-/- deficient mice.

Methods and Results: Il13ra1-/- and wild-type mice (controls) were placed on a high-fat diet at the age of 6 weeks for 18 weeks. Il13ra1-/- mice gained more weight than controls during the study period. Body composition was analyzed in-vivo using nuclear magnetic resonance (NMR). Fat-to-lean mass ratio was higher in Il13ra1-/- mice compared to controls (0.79± 0.03 and 0.63± 0.02, p<0.01). An echocardiography study was performed at the age of 24 weeks to evaluate the possible effect on cardiac dysfunction in previously characterized Il13ra1-/- mice. Surprisingly, compared with controls, high-fat diet significantly attenuated adverse LV remodeling and cardiac dysfunction in the Il13ra1-/- mice.

Conclusion: High-fat diet protects the heart of mice prone to cardiomyopathy and LV dysfunction. Our provocative findings are in line with a few previous reports suggesting that high-fat diet could attenuate or prevent LV expansion and dysfunction in response to hypertension, infarction, or genetic cardiomyopathy.









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