I heard a great talk yesterday by Dr. Patrik Rorsman from the University of Oxford, who has a new way of thinking about type 2 diabetes. He believes some individuals who develop the disease may have a deficit in insulin exocytosis, but not by the mechanism that anyone would have predicted. It is abundantly clear that type-2 diabetes is not caused by a lack of available insulin in the pancreas. Therefore, Dr. Rorsman hypothesized that the mechanism of exocytic release of insulin may be perturbed in diabetic patients. However, when he made classical measurements to detect exocytic release in primary tissues, such as amperometry of cargo release and monitoring membrane capacitance, he saw no differences between healthy and diseased cells. It wasn’t until he engineered an elegant ATP-sensitive, feedback biosensor into his recording set-up that he detected a difference in exocytosis. What he found suggests that the equilibrium between kiss-and-run and full-fusion exoc...
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