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Pancreas Size Linked to Increased Risk for Type 1 Diabetes
Finding provides new insight into disease pathogenesis (Dec. 12)
People at risk for type 1 diabetes may have fewer insulin-producing beta cells than people not at risk — a finding that could help researchers shed light on what causes the disease, according to a new study from the University of Florida.
The study — published as a letter in the December 12 issue of the Journal of the American Medical Association — found that people at risk for type 1 diabetes had smaller pancreases than did people who were not at risk.
“This is the first time this has been noted,” said Martha Campbell-Thompson, DVM, PhD. “We still don’t know what causes type 1 diabetes, but if people have fewer beta cells to begin with, other confounding factors, such as a virus or genetics, could help push them over into having clinical diabetes. There are a lot of possibilities.”
Type 1 diabetes occurs when the body’s immune system attacks its own pancreatic beta cells, which are responsible for producing insulin the body needs to convert sugar into energy. The beta cells stop producing insulin, often beginning in childhood. This differs from the more common type 2 diabetes, which often can be prevented and treated through lifestyle changes, such as improved diet and increased exercise.
In the new study, Campbell-Thompson and colleagues examined 164 pancreases from adult organ donors, including those with autoantibodies linked to an increased risk for type 1 diabetes. After comparing the organs with control samples, the researchers discovered that the people at risk for type 1 diabetes had pancreases roughly three-fourths the weight of those of patients not at risk for the disease. In addition, patients already diagnosed with type 1 diabetes had pancreases about half the weight of control samples, Campbell-Thompson said.
Obtaining and analyzing human pancreas samples has proved crucial for researchers because mouse models used to develop treatments for type 1 diabetes are no longer considered good examples of the disease in humans.
“This could really change some of the ideas we have about type 1 diabetes,” Campbell-Thompson said. “By understanding how it develops, we can think of new ways to treat it.”