Perturbed vitamin A metabolism is associated with type 2 diabetes and mitochondrial dysfunction that are linked to the development of diabetic cardiomyopathy. Importantly, the mechanism, by which vitamin A regulates mitochondrial energetics in diabetic cardiomyopathy is currently not known. To test the hypothesis that vitamin A-deficiency accelerates the onset of cardiomyopathy in diet-induced obesity (DIO), we subjected mice with Lecithin retinol acyltransferase (Lrat) germline deletion, which exhibit impaired vitamin A stores, to vitamin A-deficient high fat diet (HFD) feeding. Wildtype mice fed with a vitamin A-sufficient HFD served as controls. Cardiac structure, contractile function, and mitochondrial respiratory capacity were preserved despite vitamin A-deficiency following 20 weeks of HFD feeding. Gene profiling by RNA sequencing revealed that vitamin A is required for the expression of genes involved in cardiac fatty acid oxidation, glycolysis, tricarboxylic acid cycle, and mitochondrial oxidative phosphorylation in DIO as expression of these genes was relatively preserved under vitamin A-sufficient HFD conditions. In summary, our study identifies a transcriptional program, by which vitamin A preserves cardiac energetic gene expression in DIO that might attenuate subsequent onset of mitochondrial and contractile dysfunction.