Coaxing gut cells to make insulin: Could this be a viable treatment for Diabetes Type 1?

Diabetes type 1 can be a particularly brutal autoimmune disease that compromises the daily lives of millions of people, but researchers at Columbia University think they might have found a novel way to treat the disease. The researchers hypothesize that cells in the patient's intestine could be coaxed  into producing insulin, thereby avoiding the need for a stem cell transplant.  The research—conducted in mice—was published March 11 in the journal Nature Genetics.  The Columbia study has found that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells.  They report that when they turned off a certain gene that plays a role in cell fate decisions—Foxo1—the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.  It's interesting that turning off Foxo1 in the pancreas did not have the same result, according to the report.  Insulin-producing cells in the intestine would be hazardous if they did not release insulin in response to blood glucose levels. However,  the researchers say that the new intestinal cells have glucose-sensing receptors and do exactly that.  They note that the insulin made by the gut cells also was released into the bloodstream, worked as well as normal insulin, and was made in sufficient quantity to nearly normalize blood glucose levels in otherwise diabetic mice.

What will further research do? The key to transforming these results into a viable therapy, says Dr. Domenico Accili, MD, professor of medicine at Columbia University Medical Center, will be to find a drug that has the same effect on the gastrointestinal progenitor cells in humans as "turning off" the Foxo1 gene does in mice. That should be possible, he says, because they also discovered that they could create insulin-producing cells from progenitor cells by inhibiting Foxo1 with a chemical.