For over 15 years, researchers at the Icahn School of Medicine at Mount Sinai have been at the forefront of diabetes research, striving to identify a drug capable of inducing the regeneration of human beta cells. In a significant breakthrough in 2015, they discovered harmine, a small molecule that is capable of stimulating beta cell replication. Esra Karakose, assistant professor in the Department of Medicine, is now studying the mechanism of action, and her team’s latest publication from an in vitro study suggests that harmine is inducing “fate conversion,” where alpha cells—another type of pancreatic cell—transform into beta-like cells capable of producing insulin.ess. This is your first post. Edit or delete it, then start writing!
This revelation opens new avenues for treatment, as alpha cells are abundant in individuals with diabetes. By harnessing this potential, we may be able to address the underlying issue of beta cell loss in type 1 and type 2 diabetes.
Intriguingly, another group of researchers, including Andrew Stewart and Peng Wang, published another recent study in which they gave harmine alone or in combo with a GLP 1, to mice transplanted with human pancreatic islet cells. Harmine increased the human beta cell mass by 300% with harmine alone, and by 700% in combination with a GLP 1.
In parallel, Sana Biotechnology is pioneering a revolutionary approach to islet cell transplantation for type 1 diabetes that circumvents the need for immunosuppression. Their innovative hypoimmune technology enables the transplantation of engineered islet cells without triggering an immune response. This study represents the first instance of a successful donor-derived islet cell transplantation in a fully immune-competent individual without the need for immunosuppressive therapy.
“This person is now making his own insulin for the first time in 30 years,” said Steve Harr, the President and CEO of Sana.
Historically, the rejection of transplanted cells has posed a significant challenge in transplant medicine, necessitating lifelong immunosuppression for recipients. Sana’s approach, which includes gene modifications to create cells that evade both allogeneic and autoimmune detection, could fundamentally change the landscape of diabetes treatment. The implications of this research are profound, as it may pave the way for one-time treatments that restore insulin production in patients without the complications associated with immunosuppression.