|Gregory Steinberg and Adam Bujak, with one of their weak, AMPK-light, mice--Courtesy of McMaster U.|
Building on earlier research work, a group of researchers at McMaster University in Canada flagged a key protein as a major player in muscle loss during aging, offering a target for new drug development as well as a possible supporting role for existing diabetes medications.
Gregory Steinberg, the study's senior author and professor of medicine at the Michael G. DeGroote School of Medicine, says that a new mouse study spotlights the role of AMPK, or AMP-activated protein kinase, in supporting muscles. As people age, lower levels of AMPK are associated with muscle loss. And up to now about the only effective ways of turning on the metabolic switch for dialing AMPK activity back up has been exercise or doses of aspirin and metformin, a common diabetes drug.
"Mice lacking AMPK in their muscle developed much greater muscle weakness than we would have expected to see in a middle-aged mouse," said Steinberg in a statement. "Instead these mice, which were the equivalent of being just 50 years old, had muscles like that of an inactive 100-year-old."
The lead author of this study is Adam Bujak, a PhD student of McMaster's Medical Sciences Graduate Program. Bujak and Steinberg added that new drugs that can target the AMPK pathway could be a valuable new opportunity for drug developers.
"We know we can turn on the AMPK pathway with intense exercise and commonly-used Type 2 diabetes medications," added Steinberg. "By knowing that AMPK is vital for maintaining muscle mass with aging, we can now try to adapt exercise regimes and existing drugs to switch on AMPK in muscle more effectively. The development of new selective activators of the AMPK pathway in muscle may also be effective to prevent muscle loss with aging."
- here's the release