Low-Dose of Ethanol Intake Prevents High-Fat Diet-Induced Adverse Cardiovascular Events in Mice
Fat diet is recognized as an important player in the development of cardiovascular disease including cardiomyopathy. Besides fat diet, large-quantity ethanol also induces cardiomyopathy in both animals and humans. Emerging evidences suggest that low ethanol intake may have the protective effect on cardiovascular system. This study aimed to clarify whether low dose ethanol intake could prevent the high-fat diet induced adverse effects of cardiomyocytes in mice. After 6-8 weeks of feeding, the heart weight significantly decreased in ethanol+HFD compared to HFD mice. In addition, cardiac triglycerides and lipid droplets also decreased, but no statistically significance was found in cholesterol level between the two groups. Expression of fatty acid transporters Cd36, Slc27a1, Got2 were down-regulated in ethanol+HFD group. By echocardiography, the mass and volume of left ventricle were reduced, and the ejection fraction (EF) and fractional shortening (FS) were increased in mice fed with alcohol. Low dose ethanol reduced cardiomyocytes’ cross-sectional area and hypertrophic markers ANP and BNP expression. Moreover, Col1a1, the main collagen type expressed in the heart, was also reduced by low dose ethanol consumption. Also, the expression of Rgs5, a crucial component of the signaling pathway involved in cardiac remodeling and heart failure, was upregulated in response to ethanol intake. The data suggest that low ethanol intake prevents adverse effects induced by high-fat diet, such as lipid accumulation, cardiac dysfunction, hypertrophy and fibrosis. Furthermore, low ethanol upregulates Rgs5, which suggests its role in cardiac remodeling and heart failure.