A protein that builds up in the pancreases of baboons and leads to the suppression of insulin-producing beta cells, may provide one of the most significant indicators yet for predicting the onset of type 2 diabetes.
Researchers at The University of Texas Health Science Center at San Antonio studied pancreatic tissues from 150 baboons that had died from natural causes, including diabetes. They found that a build-up of a protein hormone called islet amyloid polypeptide (IAPP) in the islets of Langerhans contributed to the simultaneous destruction of insulin-producing beta cells and an increase in the production of glucagon, which raises blood glucose levels.
They found that IAPP acted to create this situation even when blood glucose levels were barely above normal.
Ironically, IAPP is produced by the pancreas – a seeming puzzle where the organ responsible for controlling the body’s ability to metabolize blood sugar produces a substance that thwarts that very goal.
As IAPP build-up progresses, the pancreas loses more an more beta cells to the protein’s toxic effects. In the meantime, alpha cells, which produce glucagon, proliferate. Eventually, the imbalance leads to type 2.
The proliferation of glucagon, which scientists had noted before, was something that nobody had a good explanation for. Now, with IAPP as the apparent agent, they believe they may finally have the key to glucagon over-production.
In any case, the study may have produced a marker that can tell physicians and endocrinologists that a patient is running a high risk of developing diabetes.
One advantage of the Texas study is that baboons, which are primates, are very close physiologically to humans. The monkeys can become obese and acquire type 2 diabetes and suffer from both conditions in much the same ways that humans do. In doing so, they offer researchers a fairly accurate indicator of how IAPP may affect people.
The Texas researchers published their findings in the July 20-24 online early edition of Proceedings of the National Academy of Sciences.