New research in the Journal of the American Heart Association from multidisciplinary UNC research group

A multidisciplinary team from UNC’s Departments of Nutrition, Pharmacology, Pathology, and the McAllister Heart Institute have published new findings on genetics and metabolism in the Journal of the American Heart Association.

New research in the Journal of the American Heart Association from multidisciplinary UNC research group click to enlarge New research looks at the heart's fuel sources

A multidisciplinary team from UNC’s Departments of Nutrition, Pharmacology, Pathology, and the McAllister Heart Institute have published new findings on genetics and metabolism in the Journal of the American Heart Association. The paper, “Modeling the Transition from Decompensated to Pathological Hypertrophy,” is a collaboration by Florencia Pascual (Nutrition), Jonathan C. Schisler (Pharmacology, McAllister Heart Institute), Trisha J. Grevengoed (Nutrition), Monte S. Willis (Pathology, McAllister Heart Institute), and Rosalind A. Coleman (Nutrition).

The heart, as a whole, never stops working to maintain blood circulation. This is the primary reason our heart consumes a vast amount of fuel, more than any other organ by weight, to maintain life. The healthy adult heart relies primarily on circulating fatty acids to maintain its ability to contract. In certain conditions, however, the heart can shift to other energy sources, such as glucose, protein, or ketone bodies. Some of these conditions include normal, physiological situations, such as during development and in the neonatal stage of life. However, nearly all forms of cardiac disease and heart failure are associated with a shift away from fatty acids and an increased reliance on other fuel sources. It remains unknown if this shift in energy source preference is the cause or merely a consequence of heart disease.

The researchers used a mouse that was engineered to block fatty acids as a fuel source in the heart. The researchers then studied how gene expression and metabolism change in the heart before any pathological changes occur, resulting in improved understanding of the pathways that play an important role in this transition period.

By combining studies of gene expression and metabolites along with in vivo cardiac metabolism and function, this research describes for the first time an intermediate phase of cardiac metabolism whereby alternative uses of glucose are observed in the context of long-term inhibition of fatty acid activation.