One Step Closer to an “Exercise Pill”
Suppressing a protein builds muscle mass, improves markers of heart health without weight loss
Article ID: 672858
Released: 17-Apr-2017 8:00 AM EDT
Source Newsroom: Federation of American Societies for Experimental Biology (FASEB)
Newswise — Suppressing production of the protein myostatin enhances muscle mass and leads to significant improvements in markers of heart and kidney health, according to a study conducted in mice. Joshua T. Butcher, PhD, a postdoctoral fellow at the Vascular Biology Center at Augusta University, will present the work at the American Physiological Society’s annual meeting during the Experimental Biology 2017 meeting, to be held April 22–26 in Chicago.
The researchers zeroed in on myostatin because it is known as a powerful inhibitor of skeletal muscle growth, meaning that people with more myostatin have less muscle mass and people with less myostatin have more muscle mass. Studies suggest obese people produce more myostatin, which makes it harder to exercise and harder to build muscle mass.
“Given that exercise is one of the most effective interventions for obesity, this creates a cycle by which a person becomes trapped in obesity,” Butcher said.
Obesity is linked with a range of factors that increase the risk of heart disease and diabetes, including high blood pressure, high cholesterol, insulin resistance and kidney damage. The researchers bred four groups of mice: lean and obese mice with uninhibited myostatin production and lean and obese mice that were unable to produce myostatin. As expected, mice that were unable to produce myostatin developed markedly higher muscle mass, though the obese mice remained obese even with more muscle. The obese mice that were unable to produce myostatin showed markers of cardiovascular and metabolic health that were on par with their lean counterparts and dramatically better than obese mice with uninhibited myostatin production.
“In our muscular obese mouse, despite full presentation of obesity, it appears that several of these key pathologies are prevented,” Butcher said. “While much more research is needed, at this point myostatin appears to be a very promising pathway for protection against obesity-derived cardiometabolic dysfunction.
“Ultimately, the goal of our research would be to create a pill that mimics the effect of exercise and protects against obesity. A pill that inhibits myostatin could also have applications for muscle wasting diseases, such as cancer, muscle dystrophy and AIDS,” he added.
Joshua Butcher will present this research at 12:45–3 p.m. Tuesday, April 25, in Hall F, McCormick Place Convention Center (poster E266 1011.7) (abstract). Contact the media team for more information or to obtain a free press pass to attend the meeting.
About Experimental Biology 2017
Experimental Biology is an annual meeting comprised of more than 14,000 scientists and exhibitors from six host societies and multiple guest societies. With a mission to share the newest scientific concepts and research findings shaping clinical advances, the meeting offers an unparalleled opportunity for exchange among scientists from across the U.S. and the world who represent dozens of scientific areas, from laboratory to translational to clinical research. www.experimentalbiology.org #expbio
About the American Physiological Society (APS)
APS is a nonprofit organization devoted to fostering education, scientific research and dissemination of information in the physiological sciences. The Society was founded in 1887 and today represents more than 11,000 members and publishes 14 peer-reviewed journals.
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