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Alcoholism is an addiction that needs to be treated before it leads to mental and physical illnesses. In a new study, researchers examined how long-term alcoholism can lead to muscle weakness. They discovered a link between muscle weakness caused by alcoholism and a particular mitochondrial protein.

For this study, the researchers examined mice models with mitochondrial disease. Mitochondria are organelles responsible for creating energy used in the muscle, brain and other body cells. Mitochondria's quality control over other cells in the body is highly dependent on their ability to fuse with one another. The researchers with first author Veronica Eisner, Ph.D., a postdoctoral fellow at Thomas Jefferson University developed a way to tag the mitochondria in mice's skeletal cells.

They used two different colors and observed if these organelles "mingled" with one another. The researchers concluded that the mitochondria do indeed fuse with one another and exchange contents in the process. This study showed "for the first time that mitochondrial fusion occurs in muscle cells," Dr. Eisner explained. From this part of the study, the team was able to identify Mfn1 as the most important mitofusin fusion proteins (Mfn) in skeletal muscle cells.

The researchers then set out to examine the effects of Mfn1 on muscle weakness. They discovered that the abundance of Mfn1 fell by 50 percent in the mice models that were given a regular alcohol-diet. Mitochondrial fusion also fell, while muscle fatigue increased. Other fusion proteins were not affected by alcohol.

"That alcohol can have a specific effect on this one gene involved in mitochondrial fusion suggests that other environmental factors may also specifically alter mitochondrial fusion and repair," said Dr. Gyorgy Hajnoczky, M.D., Ph.D., Director of Jefferson's MitoCare Center and professor in the department of Pathology, Anatomy & Cell Biology. "The work provides more evidence to support the concept that fission and fusion -- or mitochondrial dynamics -- may be responsible for more than just a subset of mitochondrial diseases we know of. In addition, knowing the proteins involved in the process gives us the possibility of developing a drug."

The study, "Mitochondrial fusion is frequent in skeletal muscle and supports excitation contraction coupling," was published in the Journal of Cell Biology.