Abstract
Hepatic stores of Vitamin A (retinol) are mobilized and metabolized in the heart following myocardial infarction. The physiological consequences of this mobilization are poorly understood. Here we used dietary depletion in a lecithin retinol acyltransferase mutant mouse line to induce Vitamin A deficiency and investigate the effects on cardiac function and recovery from myocardial infarction. We found that uninjured Vitamin A-depleted hearts had decreased contractile function but, paradoxically, improved recovery after injury. These effects on cardiac function were specific to male mice, which experienced more rapid and severe depletion of circulating Vitamin A. Following injury, Vitamin A deficiency also caused hepatic hypolipidemia and gene expression changes in heart and liver suggesting altered metabolism contributed to cardiac phenotypes.
Published Version
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