Unfortunately insulin needles, blood sugar monitors, alcohol swabs, band-aids, and a strict diet are also on many children's list of back-to-school items. Over 20 million children and adults in the United States are living with type-one diabetes and there is currently no cure or any preventative measures. Diabetes is a dangerously complex disease, robbing bodies of their ability to store and burn sugar. New research from the Stanford University School of Medicine may be holding an early answer to knocking those items off of that back to school list, permanently.
Stanford University's Hugh McDevitt, M.D., a microbiology and immunology professor, was one of the main authors of the study to find out how the process of type-one diabetes starts within the body. Because insulin is a main factor in all types of diabetes, the researchers were eager to figure out how the insulin cells become victims of the body's immune system which leads to the complete shut down of their production.
Without the production of insulin by the pancreas, the body doesn't get the hormone it needs to convert sugar into energy to sustain a healthy lifestyle. By not having the correct hormones in the body, a person with type-one diabetes has to learn to control their blood sugar intake and compensate for the hormone with replacement therapy, insulin shots and nutritional supplements. Type-one diabetes is most commonly diagnosed in children and young adults and was formerly known as "Juvenile Diabetes." As the leading cause of kidney failure, heart disease, amputations and blindness, diabetes is a serious condition that has now become the fifth highest cause of death in the United States alone and has become a major concern recently due to a higher obesity rate and lower activity rate among children.
In order to find out how the insulin cells were being destroyed within the body, researchers needed to isolate the one part of the equation they didn't have: how the body kills the cells. A postdoctoral microbiology and immunology scholar Dr. Qing Li, M.D., Ph.D., the primary author of the study, knew that an autoimmune attack of the pancreas was the problem but couldn't pinpoint the specific culprit. Li's study used diabetic mice to show the process of how the insulin production shuts down and what might be the trigger.
By working with the diabetic mice—who develop high blood sugar and other symptoms just like humans with diabetes—it is easier to watch and control the process of type-one diabetes because the disease is unpredictable and develops randomly within humans. Previous studies show that a type of white blood cells called CD4+ T cells, are used as an early pawn in the attack of the immune cells and that mice have more of the immune cells cells, or beta cells, within the pancreas. In normal mice, the beta cells die off on their own but in mice with diabetes, however, the dead beta cells stay in the pancreas and over time are turned into an immune signal which furthers the disease. This immune signal, known as interferon-alpha, was isolated by scientists as the trigger that slows the metabolism of the sugar and kills the insulin-producing beta cells.
Because interferon-alpha is primarily used as an aid to fight infections, the immune signal has been overlooked until now. "This was a pretty surprising finding. We never considered that interferon-alpha could be a major player in early type-1 diabetes," said Li.
The extra beta cells in the mice that died off were made active to kill the insulin-producing betas and the researchers were able to conclude that these cells were being directed by interferon-alpha. After isolating interferon-alpha as the suspect, another study was done to confirm the original findings, and the mice were given antibodies to halt interferon-alpha activity within the body a few weeks before the diabetes was predicted to take over. The antibodies delayed the start of the disease in the mice for four weeks and in 60 percent of the cases, prevented diabetes from forming altogether.
As it is with every disease trial and scientific research, the Stanford staff isn't done yet. Many more studies have to be conducted and the transference from animal to human will be hard due to outside influences of the disease on humans. For now, the discovery of the trigger for type-one diabetes is commendable. If and when diabetes does have a preventative cure, I hope that everyone will raise a glass of milk up for a toast and find a big cookie to dunk into it.
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