Loss of pancreatic β-cells or their proper function is characteristic of type 1 and type 2 diabetes, so restoring functional β-cell mass has been a major therapeutic goal in the field. A team led by Bridget Wagner at the Broad Institute's Center for the Science of Therapeutics, working with Broad associate member Rohit Kulkarni’s lab at Joslin Diabetes Center, showed that this may be achievable in humans. They found that the kinase-inhibiting enzyme 5-IT, which is known to promote β-cell mass in rodents, can also spark β-cell proliferation in humans by inhibiting the protein DYRK1A. The research, published in Diabetes, suggests a possible regenerative medicine approach to diabetes.

The human body is governed by complex biochemical circuits. Chemical inputs spur chain reactions that generate new outputs.  Understanding how these circuits work—how their components interact to enable life—is critical both to advancing basic biology and to identifying new treatments to disease, which arises when these circuits misfire. But getting to that understanding is no trivial task.