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Apelin Alleviates High Fat Diet‐Induced Cardiac Remodeling and Myocardial Contractile Dysfunction: Role of miRNA‐133a

Apelin is a novel adipokine which is thought to play a role in normal cardiovascular function and glucose homeostasis. This study was designed to examine the cardiac and metabolic effects of apelin in high fat diet‐induced obesity. C57BL6 mice were randomly assigned to receive either high‐ (45% fat) (HF) or low‐ (10% fat) (LF) fat diets starting from their 5–6 weeks of age for 20 weeks. The mice were then randomly divided to receive apelin (0.17 mg/kg, i.p./day) or vehicle for 2 weeks following which they were subjected to cardiomyocyte function assessment. HF‐diet compromised myocardial contractile function (fractional shortening, cardiomyocyte peak shortening, maximal velocity of shortening/relengthening and duration of relengthening) and intracellular Ca2+ handling, the effects of which were significantly attenuated by apelin treatment. Echocardiography revealed that increased left ventricular mass and wall thickness in HF‐fed mice, which were mitigated by apelin treatment. Western blot demonstrated that apelin treatment reduces levels of hypertrophy‐related proteins. HF‐diet reduced expression of miR‐133a, a regulator of cardiomyocyte hypertrophy, which was restored by apelin treatment. Our results suggest apelin may rescue HF‐diet‐induced cardiac hypertrophy and contractile dysfunction, which may at least in part be attributed to upregulation of miR‐133a.