Vitamin A May Protect Heart from Some Effects of Obesity

Mouse model of diet-induced obesity showed different metabolic gene expression depending on vitamin A availability

Rockville, Md. — Research in a mouse model of diet-induced obesity 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. It was chosen as an APSselect article for January.

“The present study identifies a critical role for vitamin A that preserves cardiac energetic gene expression in [diet-induced obesity].”

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.

Read the full article, “Vitamin A preserves cardiac energetic gene expression in a murine model of diet-induced obesity,” published ahead of print in the American Journal of Physiology-Heart and Circulatory Physiology. It is highlighted as one of this month’s “best of the best” as part of the American Physiological Society’s APSselect program. Read all of this month’s selected research articles.