In a surprising study, Oregon State University researchers found that no matter how much stress they placed on mice from either a high-fat diet or strenuous exercise, the animals’ mitochondria were able to adapt and continue their normal processes.
The findings could have major implications for the study of diseases like diabetes, Parkinson’s and Alzheimer’s, all of which are associated with an impairment in the breaking-down and clearance of damaged mitochondria.
Mitochondria are the structures that house cellular respiration, the process used to turn nutrients into energy. Dysfunction in mitochondria may lead to lower energy production, greater inflammation and tissue damage. Yet as central as mitochondria are to living organisms, scientists still don’t know exactly what keeps them healthy – or makes them unhealthy.
This study fits another piece into the puzzle, said Oregon State University College of Public Health and Human Sciences researcher Dr. Matt Robinson, who co-authored the paper published last week in the Federation of American Societies for Experimental Biology (FASEB) Journal with PhD student Ms. Sarah Ehrlicher.
“It helps lay some future groundwork for how we can optimize (muscle and mitochondrial) health, to promote their health with diseases like obesity, diabetes, even some implications with aging – conditions that we know have compromised mitochondria,” Dr. Robinson says. “This might provide some new pathways for how to improve the mitochondria and restore them.”Friday Letter Submission, Publish on February 14