A recent study conducted by researchers from the German Center for Diabetes Research, the Technical University of Munich and the Helmholtz Zentrum München has found a new and druggable insulin inhibitory receptor called inceptor. The study is a remarkable discovery for research on diabetes as the scientific community celebrates 50 years since the discovery of the insulin receptor and 100 years since the discovery of insulin.
The researchers found that blocking inceptor function led to increased sensitization of the insulin signaling pathway. This, they said, may allow the regeneration and protection of beta cells for diabetes remission.
Diabetes mellitus is a disease that can be identified by the dysfunction or loss of beta cells that produce insulin in a micro-organ found in the pancreas that manages systemic levels of blood sugar. The disease has many complications, such as systemic metabolic failure and chronic high blood sugar. In the long term, patients may also experience multiorgan damage, which may result in significant social and medical burdens as well as premature death.
Presently, no pharmaceutical treatment can reverse or stop the disease from progressing. Prior studies have shown that intensive insulin therapy could possibly be used to improve blood sugar control and prompt diabetes remission. However, the therapy also causes unintended weight gain and has severe side effects such as a significant risk of blood sugar deep drop, which could trigger loss of consciousness.
Heiko Lickert explained that therapies which sensitized pancreatic beta cells to insulin could potentially protect diabetes patients against failure and beta cell loss. Lickert added that with the discovery of the inceptor, his team of researchers had discovered a good molecular target for regeneration therapy and beta cell protection, which did not carry the severe side effects of intensive insulin therapy.
The researchers conducted experiments with mice and found that the inceptor’s function was to protect the beta cells, which produce insulin, from activation of the insulin pathway. They also found that the inceptor-blocking insulin signaling may contribute to insulin resistance, in addition to being overexpressed in diabetes.
To learn what happened when the inceptor’s function was hindered pharmacologically or genetically, the researchers used monoclonal antibodies to block the inceptor’s function then eliminated the inceptor in beta cells. The report noted that researchers found that the functional beta cell mass and insulin signaling increased, which made the inceptor a good molecular target to treat the dysfunction and loss of beta cells as well as the root cause of diabetes. The study was published in “Nature”.
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