Researchers have discovered that muscle weakness can result from a mutated mitochondrial fusion gene, which also contributes to diseases such as Autosomal Dominant Optical Atropy and Charcot-Marie-Tooth disease. Mitochondria are essential to the human body because they provide energy for all cells. By fusing with one another, mitochondria can swap dysfunctional proteins for functioning ones. This ensures that the mitochondria throughout the body are continuously functioning properly.
In order to determine whether mitochondria can repair themselves in skeletal muscle, Veronica Eisner, Ph.D., created a scenario in which mitochondria were tagged in skeletal muscle of rats with varying colors to observe whether they were able to fuse. Her research concluded that mitochondria in skeletal muscles were able to fuse with both nearby mitochondria as well as mitochondria located further away in muscle cells. A research team led my Dr. Gyorgy Hajnoczky expanded on this discovery by linking mitofusion protein Mfn1 to muscle weakness. Because muscle weakness can result from alcoholism, the team performed an experiment with rats that were given an alcoholic diet, and determined that both the number of Mfn1 proteins and the amount of mitochondrial fusion decreased due to alcohol. Mitochondrial fusion then increased when Mfn1 was increased.
Thus, alcohol likely has a detrimental effect on the Mfn1 gene, which then inhibits mitochondrial fusion and leads to weakened muscles. The newfound knowledge of the Mfn1 protein does, however, provide promise for future developments of drug treatments.
Reference:
Thomas Jefferson University. (2014, April 21). Why alcoholism saps muscle strength. ScienceDaily. Retrieved May 15, 2014 from www.sciencedaily.com/releases/2014/04/140421093725.htm
Posts
