Similarly, the mice receiving rosiglitazone actually gained weight in this study, as did the mice without tumors. The mice with tumors receiving no treatment lost fat tissue, suggesting they were experiencing the onset of cachexia despite the high-fat diet they were eating.
In addition to stopping fat and muscle loss, the rosiglitazone also dramatically reduced two biological markers present when proteins break down, particularly in muscles, and a third marker that indicates cells are eating their own amino acids in an attempt to survive.
"We found that those markers of protein and muscle degradation are increased in mice with cachexia, and then when we gave them rosiglitazone, that significantly slowed that degradation," Belury said.
It's too soon to know whether the same drug would have the same effect on humans with cancer, Belury noted. Not all people with cancer develop cachexia, and it's difficult to catch cachexia before severe weight loss has already occurred. And by the time muscles begin to break down, the entire body reacts to the release of amino acids, meaning treatment at that time would have to take such reactions into account.
"For this research, we wanted to catch cachexia as it was having an influence on muscle wasting without the wasting muscle having an influence back on the cachexia," Belury said.
In future studies, the scientists plan to further test the timing and dosage of rosiglitazone and other insulin sensitizers to see if the experiments produce a "prominent, universal effect," Belury said.
|Contact: Martha Belury|
Ohio State University