Seung Kim didn’t set out to shake up the world of diabetes research. But he may have hit on a crucial regulator.
An assistant professor of developmental biology at the School of Medicine, Kim, MD ’92, PhD ’92, knew that some immunosuppressants, like those taken by organ transplant patients, inhibit production of the protein calcineurin and increase the risk of developing diabetes. Kim, MD/PhD student Jeremy Heit and professor of pathology Gerald Crabtree suppressed calcineurin production in infant mice.
Within 12 weeks, the mice were severely diabetic. Suppressing calcineurin prevented insulin-producing pancreatic beta cells from increasing in number, which was necessary to metabolize sugar as the mice grew. It also reduced the amount of insulin made by their existing beta cells.
Heit and Kim further experimented by artificially activating NFAT, calcineurin’s protein “sidekick.” Beta cells that did not have calcineurin but had active NFAT produced the appropriate amounts of insulin. If Kim’s findings, published in the September 21 issue of Nature, are verified in humans, they could lead to new treatments for diabetes, hypoglycemia and some pancreatic tumors.
