A study done at Ohio State researched a new treatment for heart failure that targets metabolic protein relationships.
The study, published in the journal Circulation, details a key chemical process in hearts that could be targeted to improve their metabolic function and reduce the symptoms of the disease.
Dr. Doug Lewandowski, director of translational research at Ohio State’s Dorothy M. Davis Heart and Lung Research Institute, said the key to the study was looking at the heart’s metabolism.
“Our lab studies how [the heart] fuels itself, and how it converts carbon-based fuels like fats and sugars in the energy it needs to support that contractile function,” Lewandowski said.
Heart failure, a fatal disease that affects about 5.7 million adults in the U.S. and costs the country an estimated $30.7 billion annually, occurs as heart metabolic function begins to decline, according to the Center for Disease Control.
Lewandowski’s study, which also involved researchers at the University of Illinois, Columbia University and Friedrich Schiller University Jena in Germany, investigated the relationship between heart failure and acyl CoA, an important protein that facilitates fat metabolism.
“Hearts really run on fat,” Lewandowski said. “Normally, the heart knows what to do with that fat. It burns it up, because it’s an energy-rich source.”
However, heart failure interferes with the acyl CoA protein, leading to issues with fat metabolism and causing great physiological stress for the organ.
“In the failing heart, there’s a loss of the long chain acyl CoA,” Dr. Joseph Goldenberg, lead author of the study and current resident at the University of Chicago, said. “The consequence is that in the failing heart, there’s less fatty acids available to the actual muscle cell of the heart, and that results in less fatty acids being oxidized for energy.”
Not only does the decrease in acyl CoA reduce fat metabolism, it also leads to the production of toxic fats, a phenomenon called lipotoxicity. The study showed that restoring acyl CoA in mice with heart failure not only improved heart metabolic function, but also reduced lipotoxicity, leading to overall greater heart health.
According to Lewandowski and Goldenberg, the next step is to learn how to apply these findings to humans. They said this could potentially be done through drugs, gene therapy or even nutritional supplements.
Lewandowski said that although the treatments for heart disease in general have improved in America, heart failure has not decreased in the past 35 years.
“We’ve made tremendous advances in reducing the incidence of heart disease in America,” he said. “People think, ‘OK, that’s done, let’s move on to something else. Just don’t eat at McDonald’s every day.’ It’s not that simple.”