The insulin-producing beta cells in the pancreas become less able to replicate with age, and the incidence of type 2 diabetes goes up. Inducing replication of endogenous beta cells is a goal for treating type 2 diabetes.
Maureen Gannon, Ph.D., and colleagues examined the role of the transcription factor FoxM1, which is required for beta cell replication in various situations, in aged beta cells.
They found that induction of an activated form of FoxM1 in aged mice increased beta cell mass and proliferation after just two weeks. They also showed that activated FoxM1 in young mice improved glucose balance without changing beta cell mass and that isolated islets missing FoxM1 had reduced insulin secretion. Together, the findings suggest that FoxM1 improves both beta cell proliferation and function.
The results, reported in the journal Diabetes, demonstrate that activated FoxM1 can counteract the age-related decline in beta cell replication and improve glucose balance, making it an attractive therapeutic target for diabetes.
This research was supported by the U.S. Department of Veterans Affairs and the Juvenile Diabetes Research Foundation.
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