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Newswise New York, NY (June 30, 2014) By switching off a single gene, scientists at Columbia Universitys Naomi Berrie Diabetes Center have converted human gastrointestinal cells into insulin-producing cells, demonstrating in principle that a drug could retrain cells inside a persons GI tract to produce insulin.

The new research was reported today in the online issue of the journal Nature Communications.

People have been talking about turning one cell into another for a long time, but until now we hadnt gotten to the point of creating a fully functional insulin-producing cell by the manipulation of a single target, said the studys senior author, Domenico Accili, MD, the Russell Berrie Foundation Professor of Diabetes (in Medicine) at Columbia University Medical Center (CUMC).

The finding raises the possibility that cells lost in type 1 diabetes may be more easily replaced through the reeducation of existing cells than through the transplantation of new cells created from embryonic or adult stem cells.

For nearly two decades, researchers have been trying to make surrogate insulin-producing cells for type 1 diabetes patients. In type 1 diabetes, the bodys natural insulin-producing cells are destroyed by the immune system.

Although insulin-producing cells can now be made in the lab from stem cells, these cells do not yet have all the functions of naturally occurring pancreatic beta cells.

This has led some researchers to try instead to transform existing cells in a patient into insulin-producers. Previous work by Dr. Accilis lab had shown that mouse intestinal cells can be transformed into insulin-producing cells; the current Columbia study shows that this technique also works in human cells.

The Columbia researchers were able to teach human gut cells to make insulin in response to physiological circumstances by deactivating the cells FOXO1 gene. Accili and postdoctoral fellow Ryotaro Bouchi first created a tissue model of the human intestine with human pluripotent stem cells. Through genetic engineering, they then deactivated any functioning FOXO1 inside the intestinal cells. After seven days, some of the cells started releasing insulin and, equally important, only in response to glucose.

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