A proof-of-concept study demonstrates that ductal cells derived from the human pancreas can be influenced by pharmacological stimulation to regenerate beta-like cells that functionally release insulin, providing new hope for people living with diabetes.
, conducted by Safiya Naina Marikar from the Baker Heart and Diabetes Institute and published in the journal, demonstrates how drugs can influence pancreatic progenitor cells to reactivate into beta-like producing insulin cells by inhibiting the EZH2 enzyme.
With type 1 diabetes, beta cell damage and destruction mean the pancreas produces little or no insulin. This results in glucose build up in the bloodstream instead of going into the cells. This build-up of glucose in the blood is called hyperglycemia, with the body unable to use the glucose for energy.
Researchers have dedicated enormous time and energy looking at alternatives such as cell replacement therapy and pancreas transplantation—a potential option limited because of the stark reality of donor organ shortage. This approach examines the regenerative capacity of pancreatic cells by stimulating ductal stem cells withas an alternative strategy to restore insulin production for people living with diabetes.
The drugs used in the study include a synthetically designed drug primarily used as a cancer therapeutic and a naturally derivedPh.D. student at Monash University, Safiya Naina Marikar, who is based at the Baker Institute in Professor Sam El-Osta's Human Epigenetics program, says this study suggests that the reprogrammed cells are capable of producing insulin and critical functionality such as
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