Can the loss of functional beta cell mass in T1D be reversed to restore insulin production? That is a fundamental question for those working to eliminate the disease; and JDRF is supporting research that could provide some answers.
Unlike some other cells in our bodies, insulin-producing beta cells don’t replicate readily, especially as we age. That’s a problem for researchers who are working to cure T1D by rebuilding functional beta cell mass lost to autoimmune attacks. But some investigators have noticed that, with the right encouragement, other islet cells can change identity and take on the characteristics of beta cells, including insulin production. JDRF is supporting several projects seeking to exploit that ability, hoping to regenerate beta cell mass. Two JDRF-funded investigators recently announced they’d found ways to chemically stimulate pancreatic alpha cells—the cells that normally produce glucagon—to change into insulin-producing beta-like cells. French researcher Patrick Collombat, Ph.D., found that GABA, a naturally occurring chemical and common dietary supplement, triggers the conversion of mouse alpha cells into beta-like cells. Treating diabetic mice with GABA fully restored beta cell mass and reversed their diabetes, and human islets transplanted into mice appeared to respond in the same way as the mouse islets. Investigator Stefan Kubicek, Ph.D., at the Austrian Academy of Sciences realized similar results using a type of FDA-approved anti-malarial drugs called artemisinins. These results suggest it may be possible to “retrain” alpha cells that continue to survive in the pancreas of a person with T1D into insulin-producing cells, a critical step toward a cure.
Next steps for both investigators include working to better understand the processes and mechanisms underlying the alpha-to-beta cell changes, which could help identify improved compounds that are able to trigger the same alterations. Continued research could also enable them to determine how best to use these compounds to treat the disease. They’ll also investigate whether the changed cells can reliably reverse mouse models of T1D. Most importantly, these compounds, which are already in use in humans, may be moved quickly into clinical testing for the treatment of T1D. Restoring functional beta cell mass and renewing the body’s ability to produce insulin is a high priority for JDRF because it would reduce or eliminate the daily burdens and hazards of managing blood-glucose levels. Even partial restoration or maintenance of beta cell function could offer significant benefits to people with T1D, including slowing or preventing progression of the disease, reduced insulin requirements, improved glucose control and a lower risk of complications. Find out more about JDRF’s Beta Cell Restoration Program at jdrf.org.
Why is this important?
Restoring the body’s ability to produce insulin will enable people with T1D to more easily manage their blood-glucose levels and may ultimately provide a cure for the disease. To do that, it’s necessary to have a sufficient number of functional beta cells, whether they’re naturally produced, chemically transformed or implanted. Once we find ways to restore and protect functional beta cell mass, the burdens, limitations and fears associated with T1D become things of the past.