A new study led by Dr. Sandy Williams, dean of the School of Medicine, could lead to a drug that mimics the benefits of exercise. But coach potatoes may not want to celebrate just yet, as the research has only begun to identify targets for the development of new drugs.
The study, which debuted in the Apr. 12 edition of the journal Science, identified a biochemical pathway in muscle cells responsible for generating many of the beneficial effects of regular exercise, and the news has made national headlines.
"We think this discovery could lead to the synthesis of new drugs that will allow individuals to acquire the health benefits of regular exercise, even if they cannot exercise," Williams said in a statement. "It has the potential to improve the lives of patients with heart failure, pulmonary disease, renal failure, diabetes and other chronic diseases."
The researchers hope to synthesize a drug to replicate the biochemical pathways, thereby inducing the benefits of exercise.
Frederick Thurmond, a postdoctoral research fellow at the University of Texas Southwestern Medical Center in Dallas and a co-author of the study, said that because the study involved genetic manipulation of mice instead of human drug therapy, finding a human application for the research may present problems.
"We have no easily deliverable drugs that can do that," Thurmond said. "So theoretically, it's possible, but whether it ever happens or not, the technology doesn't exist right now."
Williams co-authored the study with several researchers from the Southwestern Medical Center, where he served as chief of the cardiology division before his appointment last spring as the dean of Duke's medical school.
In 1998, the team found that a signaling protein, calcineurin, could mimic some of the effects of endurance exercise. The new research, however, found another pathway at the cellular level that involved another group of signaling proteins, called calmodulin-dependent protein kinases. These proteins control genes that influence the physiological and metabolic properties of muscles.
"The pathways leading to muscle development and overdevelopment are still not very clearly defined," Thurmond said. "Being able to induce what appears to be an exercise muscle by overstimulating a biochemical pathway is significant."
The study used genetically-altered mice, which produced a continuously active version of the CaMK enzyme--which controls the production of mitochondria, structures in muscle cells that often increase in number when an individual exercises regularly. The mice, although sedentary, had assumed muscular characteristics similar to those of animals that exercised regularly.
"We took muscles that fatigue easily, introduced one activated protein and we were able to change the muscle to appear exercised," said Dr. Rhonda Bassell-Duby, associate professor of cardiology at Southwestern.
As the study at Duke continues to develop drug targets, Williams will also try to determine whether the pathway applies to fat and other tissues or even to cancer cells.
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