STANFORD, Calif. - Scientists at the Stanford University School of Medicine are shedding light on how type-1 diabetes begins.
Doctors have known the disease is caused by an autoimmune attack on the pancreas, but the exact trigger of the attack has been unclear. Now, a new study in mice implicates the immune signal interferon-alpha as an early culprit in a chain of events that upend sugar metabolism and make patients dependent on lifelong insulin injections.
"We never considered that interferon-alpha could be a major player in early type-1 diabetes," said Qing Li, MD, PhD, a postdoctoral scholar in microbiology and immunology who was the primary author of a paper describing the new result. The study is published in today's issue of Proceedings of the National Academy of Sciences. "This was a pretty surprising finding."
Interferon-alpha normally helps the body fight viruses. Synthetic interferon-alpha is injected as a drug for treating hepatitis C and some forms of cancer, Li noted.
"Everybody's been wondering what process initiates type-1 diabetes," said Hugh McDevitt, MD, professor of microbiology and immunology and the study's senior author.
Type-1 diabetes is caused by complete deficiency of insulin, a hormone that helps the body store and burn sugar. About 1 million Americans have the disease, also known as juvenile diabetes because it tends to be diagnosed in children and young adults, for which there is no effective prevention or cure. Diabetes is a leading cause of heart disease, blindness, limb amputations and kidney failure.
The early pathology of type-1 diabetes is hard to study in humans, McDevitt said, because it's almost impossible to predict who will get the disease and when it will develop. Scientists have relied on animal models, such as diabetic mice, because they predictably develop high blood sugar and other features of the human disease.
To pinpoint interferon-alpha, Li a
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Stanford University Medical Center