In a surprising turn during their research on pancreatic cancer, University of Pittsburgh scientists Dr. Farzad Esni and Dr. Jing Hu discovered an unexpected potential treatment for diabetes.
While studying the effects of deleting a gene responsible for producing an enzyme called focal adhesion kinase (FAK) in mice, they observed unusual changes in the pancreas that suggested regeneration activity.
Dr. Esni, an associate professor of surgery and a member of various research institutes at Pitt, noted that the pancreas of the genetically altered mice displayed signs of attempting to regenerate, akin to a response to injury.
More intriguingly, they found a cluster of pancreatic cells simultaneously producing insulin and amylase—a phenomenon not observed under normal conditions, as insulin is typically produced by beta cells, and amylase by acinar cells.
This led the researchers to investigate whether acinar cells could be reprogrammed to produce insulin, a discovery that could revolutionize diabetes treatment. Their subsequent research, published in Nature Communications, confirmed this possibility.
They found that a drug initially developed for cancer treatment, which inhibits FAK, could induce acinar cells to transform into insulin-producing cells in diabetic mice.
The study employed the FAK-inhibiting drug PF562271, previously tested in phase 1 cancer trials, making it a potentially quicker candidate for clinical diabetes treatment due to its existing data on human safety.
The drug was administered orally, which offers simplicity over more complex genetic manipulation methods.
In their experimental model, diabetic mice treated with the FAK inhibitor not only showed a significant increase in their pancreatic beta cell mass—about 30% of their original mass—but also demonstrated improved control over their blood sugar levels.
The effects were long-lasting, suggesting that a single treatment course could have prolonged benefits.
This groundbreaking approach was also tested in a non-human primate model, where one diabetic macaque treated with the FAK inhibitor saw a 60% reduction in its insulin needs six weeks post-treatment, a stable improvement that persisted throughout the four-month study period.
The researchers are excited about the implications of these findings, as they suggest a new therapeutic pathway that could replace or reduce the need for insulin therapy in diabetics, thereby mitigating the risk of complications associated with high blood sugar levels such as heart attacks and strokes.
Dr. Esni highlighted the unique advantage of the newly identified acinar-derived insulin-producing (ADIP) cells, which not only mimic the insulin-producing capability of beta cells but also integrate into the existing pancreatic islet structures.
This integration allows them to efficiently monitor blood glucose levels due to their proximity to blood vessels.
Looking ahead, the team plans to extend their research to long-term experiments in mice to explore the sustainability of hyperglycemia control with the FAK inhibitor and to examine the effects of this treatment on human pancreatic tissues.
The ultimate goal is to progress to clinical trials to test this promising therapy in diabetic patients, potentially offering a new, effective treatment option.
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The research findings can be found in Nature Communications.
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