A surprising finding is how central calcineurin turns out to be in the health and happiness of the insulin-producing pancreatic beta cells. Drugs based on this research could potentially expand the numbers of the few beta cells that remain in diabetics and make those cells perform better. “That would have a major impact on the lives of people with diabetes.”
The implications of these findings are many:
* Drugs that enhance the activity of calcineurin or NFAT could become a new treatment for type-2, or adult-onset diabetes, in which the beta cells don’t produce enough insulin.
* Drugs that inhibit calcineurin or NFAT could treat diseases in which the beta cells produce too much insulin, such as hypoglycemia or some pancreatic tumors.
* Treating isolated beta cells with drugs that enhance calcineurin could make those cells divide, producing more cells for transplantation.
* Activating calcineurin could help Kim in his efforts to direct embryonic stem cells to become insulin-producing cells.
Kim, whose work in diabetes includes the development of islet cells, identifying new drug targets and potential stem cell treatments, said the calcineurin findings have wide-ranging implications. “The finding that the calcineurin pathway regulates other pathways in the beta cell makes it highly relevant to many areas of diabetes research,” he said.
Campbell said the next step is to verify that the findings in mice also hold true in humans.