Alterations in our response to the taste or smell of food may be another culprit responsible for Type 2 diabetes, according to scientists at Duke University Medical Center who have identified the specific mechanism in human specimens and in mice.
When we anticipate or smell a meal, the parasympathetic nervous system triggers salivation and increases insulin production in response to the expectation that glucose will be entering the blood stream.
"We think this parasympathetic response is potentially important in type 2 diabetes," said Vann Bennett, the James B. Duke professor in the departments of cell biology, biochemistry, and neurobiology and Howard Hughes Medical Institute investigator. "Our study showed there is a novel mutation in the gene encoding ankyrin-B, which increases the risk of type 2 diabetes. This happens through an impairment of the insulin secretion that is added by the parasympathetic nervous system."
The study was released online on Tuesday, March 16 in Science Signaling.
Bennett was the first scientist to delineate a molecule called ankyrin and for years has been studying its roles in the heart and brain, as well as other organ systems. Bennett and colleagues discovered the importance of ankyrin-B in the insulin response and the source of a mutation that could lead to diabetes.
In earlier experiments, the group found that pancreatic beta cells that are ankyrin-B deficient display impaired insulin secretion in mice. Ankyrin-B-deficient mice had high blood sugar after eating a source of glucose, but not if the glucose bypassed the mouse's mouth. These findings indicated that ankyrin-B deficiency impaired the parasympathetic chain of events that enhance insulin secretion and had a measurable impact on blood sugar levels.