Scientists Find One Cause of Type II Diabetes, Bring Cure Closer
A new aspect and possible cause of diabetes has been identified that could guide medical science towards new treatment for the disease. Researchers at the world’s largest diabetes research center noticed that at least half in people with Type II diabetes had diminished levels of an enzyme found in the skeletal muscles of healthy people. This suggests drugs might be developed to boost this enzyme to fight diabetes.
Sirt3 is a multi-purpose enzyme found in the mitochondria, the cellular “power plants” that process energy, turning it into a form cells can use for power. Sirt3 also works to suppress tumors, and studies have shown mice deprived of this enzyme develop mammary cancers. The sirtuin groups of proteins have a number of molecular functions in humans, including roles in stress resistance, aging and metabolic management.
Scientists at the JoslinDiabetesCenterin Boston, Massachusetts, published their findings online, saying that the lack of Sirt3 in people and animals with diabetes may promote insulin resistance, one of the earliest symptoms of the disease. Insulin is a hormone produced by the pancreas as a “messenger” to stimulate the body’s tissues to take up glucose from the bloodstream after eating. In diabetics, the cells become slow to respond to the insulin and glucose is left in the bloodstream, which can cause damage to cells and organs over time. Previous studies have shown that the mitochondria do not work properly in diabetics, and now researchers believe the decreased amount of Sirt3 in diabetics may be responsible. The Sirt3-deficient mitochondria release reactive oxygen species, reactive molecules that cause insulin resistance in the muscle tissues.
The study, published in August 2011, suggests that the future scientific goal in diabetic research will be discovering a way to restore Sirt3 levels in the mitochondria of diabetics. This will help decrease insulin resistance in diabetics, and could save patients from the many serious long-term side effects of the disease. These can include heart disease, eye problems, and neuropathy leading in severe cases to loss of feeling in the extremities, kidney failure, and strokes.
A drug or therapy to improve Sirt3 levels could also useful in the treatment of people with pre-diabetes, the condition leading to the disease, and may even prevent them from going on to develop full diabetes. More than 79 million people in the US are diagnosed as having pre-diabetes and doctors believe the total number may be even higher. Increasing Sirt3 levels could also alleviate or even reverse symptoms in people with full Type II diabetes.
Dr. Ronald Kahn, head of theJoslinCenter’s Integrative Physiology and Metabolism section, commented that this was the first study to show a single factor, which affects mitochondrial metabolism and insulin performance in the body. He said further study will need to be done, particularly to find out which proteins are affected by Sirt3. “It is a new target,” he said.
Co-author Dr Eric Verdin of the Gladstone Institute of Virology and Immunology and theUniversityofCalifornia, spoke of the importance of discovering the many roles of Sirt3 in order “to better combat this widespread disease at the cellular level.”
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