According to Duke University researchers, a mutation that causes the lack of an insulin-controlling molecule may be a factor in the development of type 2 diabetes. The molecule, ankyrin B, is activated in response to the smell and taste of food and leads to the production of insulin in preparation for food intake.
Because ankyrin B is an important factor in the body’s insulin response, researchers at Duke University Medical Center experimented with genetically mutated lab mice to see how they were affected by a deficiency of the molecule. They found that a lack of ankyrin B impaired the mice’s ability to produce proper amounts of insulin in response to food smells and tastes. This led to higher blood glucose levels, which over time led to the onset of type 2 diabetes.
Based upon the sequence of events-ankyrin B deficiency, followed by long-term effects on blood sugar levels, followed by diabetes-the Duke researchers concluded that the disease gradually develops through the parasympathetic nervous system*, not as a result of the foods eaten by the mice. In other words, the persistent inability to secrete proper levels of insulin was an effect of a genetic mutation rather than of eating the “wrong” foods.
As the researchers investigated further into the implications of ankyrin B deficiency, they found that one ankyrin B mutation was associated with type 2 in whites and non-white Hispanics. These findings open the door to research into genetic therapies that could help prevent the onset of type 2 in certain populations.
The study was published online in the March 11 edition of the journal Science Signaling.
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* The part of the autonomic nervous system that, among other things, increases intestinal and glandular activity, and stimulates digestive secretions.
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