by In a groundbreaking discovery, researchers from the University of Pittsburgh, led by Dr. Farzad Esni and Jing Hu, have found that deleting one of the two copies of the gene encoding the enzyme focal adhesion kinase (FAK) in mice led to an unexpected outcome. Instead of advancing their research on pancreatic cancer, they stumbled upon a phenomenon that could potentially revolutionize diabetes treatment.
The pancreas of the mutant mice exhibited an unusual appearance, resembling regeneration after an injury. Esni, an associate professor of surgery at Pitt and a member of UPMC Hillman Cancer Center and the McGowan Institute for Regenerative Medicine, described the scene as “weird.”
A group of cells within the pancreas displayed a peculiar trait: they expressed both insulin, the hormone responsible for regulating blood sugar, and amylase, a digestive enzyme. In normal conditions, insulin is produced by beta cells, while amylase is manufactured by acinar cells. The distinct functions of these two cell types made this observation intriguing.
Three possible explanations arose from this finding. It could have been an experimental artifact, beta cells might have started producing amylase, or acinar cells could have started generating insulin. Esni and his team were thrilled to find that the latter was indeed the case.
In a recent study published in Nature Communications, the researchers demonstrated that a FAK-inhibiting drug, which has previously been explored for cancer treatment, could transform acinar cells into acinar-derived insulin-producing (ADIP) cells. This drug-induced conversion helped regulate blood glucose levels in diabetic mice and even in a single non-human primate. This discovery could pave the way for a novel approach to diabetes treatment.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
