ArticleAmerican journal of physiology. Heart and circulatory physiology2022
Vitamin A preserves cardiac energetic gene expression in a murine model of diet-induced obesity.
Article in American journal of physiology. Heart and circulatory physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Peripartum-Associated Heart Failure Develops Independently of RHOT Proteins.International journal of molecular sciences · 2026Article
- RHOT Proteins Link Mitochondrial Motility to Cardiomyocyte Sarcomere Maturation.Circulation research · 2026Article
- Dietary Fat Intake Attenuates Vitamin A Deficiency-Associated Elastic Fiber Remodeling and Lipid Reduction in the Alveolar Niche in Mice.The Journal of nutrition · 2025Article
- Vitamin A deficiency and male-specific effects on heart function in mice.Biochemical and biophysical research communications · 2025Article
- Vitamin A deficiency attenuates cardiac rupture inFrontiers in cardiovascular medicine · 2025Article
- Realistic Aspects of Cardiac Ultrasound in Rats: Practical Tips for Improved Examination.Journal of imaging · 2024Review
- Hypoxia Attenuates Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2024Article
- Vitamin A regulates tissue-specific organ remodeling in diet-induced obesity independent of mitochondrial function.Frontiers in endocrinology · 2023Article
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
Perturbed vitamin-A metabolism is associated with type 2 diabetes and mitochondrial dysfunction that are pathophysiologically linked to the development of diabetic cardiomyopathy (DCM). However, the mechanism, by which vitamin A might regulate mitochondrial energetics in DCM has previously not been explored. 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. Wild-type 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 wk 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. Together, these data identify a transcriptional program, by which vitamin A preserves cardiac energetic gene expression in DIO that might attenuate subsequent onset of mitochondrial and contractile dysfunction.
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