Researchers from the University of Munich have discovered a novel and druggable insulin inhibitory receptor, named inceptor. The blocking of inceptor function leads to an increased sensitization of the insulin signaling pathway in pancreatic beta cells. Their study was published in Nature.
Heiko Lickert's research team focuses on the development of regenerative approaches to treat diabetes complementary and alternative to the classical immunological and metabolic therapies. "Insulin resistance in pancreatic beta cells causes diabetes. Therapies that sensitize those cells to insulin may protect patients with diabetes against beta cell loss and failure,” says Lickert.
In experiments with mice, the researchers showed that the function of inceptor is to shield the insulin-producing beta cells from constitutive insulin pathway activation. The group knocked out an inceptor in beta cells and by blocking its function using monoclonal antibodies. "The result was exactly what we were hoping for: Insulin signaling and the functional beta cell mass was increased. This makes inceptor a very promising target to treat the root cause of diabetes, the loss and dysfunction of beta cells," Lickert adds.
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"Frederick Banting noted already in his Nobel Prize lecture for the discovery of the life-saving drug insulin a hundred years ago that 'Insulin is not a cure for diabetes, but a treatment of the symptoms'. This has not changed in the last century. Our goal for future research is to leverage on the discovery of inceptor and develop drugs for beta cell regeneration. This could be beneficial for patients with type 1 and 2 diabetes and ultimately lead to diabetes remission,” states Lickert.