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Research in a mouse model of diet-induced obesity has found greater disruption to genes involved in heart function when coupled with vitamin A deficiency using a combined dietary and genetic approach. The study is published ahead of print in the American Journal of Physiology-Heart and Circulatory Physiology.
The research team, based at Hannover Medical School in Germany, induced obesity in a mouse model of vitamin A deficiency. After 20 weeks, the researchers compared the hearts and metabolism of the mice to obese mice with sufficient levels of vitamin A. In comparison, the vitamin-deficient obese mice had repression of genes in the heart that are associated with extracting energy from fat, extracting energy from glucose, and the production of the energy-carrying molecule adenosine triphosphate.
All of these areas are critical to metabolic functioning.
“Our study identifies a role for vitamin A in preserving cardiac energetic gene expression that might attenuate subsequent development of mitochondrial and contractile dysfunction in diet-induced obesity,” the researchers wrote.
American Physiological Society