Breakthrough in cell regeneration offers new hope for diabetes

In a groundbreaking development, researchers have discovered a method to regenerate insulin-producing cells in the pancreas, potentially revolutionizing diabetes treatment. This breakthrough, spearheaded by the Baker Heart and Diabetes Institute in Australia, involves repurposing FDA-approved drugs to stimulate the growth of pancreatic ductal progenitor cells, which can mimic the function of β-cells typically impaired in type 1 diabetes.

The study centers on two drugs, GSK126 and Tazemetostat, originally approved for cancer treatments. These drugs target the EZH2 enzyme, a key regulator of cell development, and by inhibiting this enzyme, the researchers were able to reprogram pancreatic ductal cells to produce and secrete insulin in response to glucose levels, akin to β-cells. This discovery is particularly significant for type 1 diabetes, where the immune system erroneously destroys β-cells, necessitating regular insulin injections to manage blood glucose levels.

The research revealed that it only took 48 hours of drug-induced stimulation for regular insulin production to resume in tissue samples from individuals with and without diabetes, spanning various ages. Given the global prevalence of diabetes, affecting approximately 422 million people, this innovative approach offers a potential alternative to the constant monitoring and management of blood sugar levels. However, the research is still in its early stages, with clinical trials yet to commence.

This advancement is not isolated; it forms part of a broader spectrum of scientific explorations into diabetes treatment, including new drug developments and strategies to protect insulin-producing cells before their destruction. Epigeneticist Sam El-Osta, from the Baker Heart and Diabetes Institute, highlights the importance of this regenerative approach for future clinical applications, emphasizing the need to understand the epigenetic mechanisms driving such regeneration in humans. The full details of this research have been published in Signal Transduction and Targeted Therapy.