Discovery of New Gene May Prevent Muscle Problems in the Future
Individuals who suffer from diabetes, particularly those with type 2, or insulin resistant, diabetes, know that muscle pain can be a major problem when it comes to dealing with the disease. However, many do not realize that their muscles can also begin to waste away, a biological process known as atrophy, which results from disuse of the muscles in question. A new discovery by a team at the Garvan Institute of Medical Research, located in Sydney, Australia, may mean that diabetes patients no longer have to suffer from this unfortunately common muscle problem.
Muscular atrophy, while one of the more common problems associated with diabetes, is not as severe as muscular dystrophy, which results in damage and weakening of the muscles. This problem occurs for those with diabetes, especially type 2 diabetes, because the body can no longer regulate glucose levels properly. Because the muscles use more glucose than any other part of the body, this lack of regulation negatively affects the muscles. The team from Sydney used this premise to begin their research, hoping they would find a way to assist muscles in dealing with the glucose and insulin levels associated with type 2 diabetes. What they found, though, may actually result in the prevention of the problem altogether.
By studying mice, the team discovered a gene, which may allow medical practitioners to alter the number of muscle fibers in a patient’s muscles in the future. As of yet, the gene, known as Grb10, allowed scientists to alter these fibers while the mice were still in an embryonic stage by reducing the amount of the gene in the animal’s embryo. This alteration of muscles is a completely new method of creating larger muscles. In the past, the method used was simply increasing the size of the muscle fibers rather than the number of them.
The researchers believe that this discovery can apply to regeneration of muscles in general as well as improve muscle capacity for those with diabetes. The first includes just about any instance of muscle atrophy, such as when a patient has not used a particular set of muscles in several weeks after breaking a bone and being treated with a cast. The other applies to muscle dystrophy. Theoretically, doctors could increase muscle mass for these patients, allowing for the stronger muscles the person may have had prior to dystrophy. This also allows efficient transfer of glucose from the blood stream to cells in muscles, which is one of the major goals of diabetes treatments in general.
Although many diabetes patients suffer from muscle problems, the majority of those with diabetes do not. However, the potential benefit from further research on the Grb10 gene is obvious, and the team from Sydney, as well as many others around the world will continue. In the future those with muscle problems, with or without diabetes, may no longer be as limited as they are now, allowing them to live out their lives just like everyone else.
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