> Diabetes Research > Mouse Sut shows new way to treat Type 1 Diabetes

Mouse Sut shows new way to treat Type 1 Diabetes

Mice—generally regarded as pests—may actually hold the key to curing diabetes within their gut.

Researchers at the Columbia University Medical Center discovered that cells in the intestine of mice can be coaxed into producing insulin, by blocking a certain type of gene. Professor of Medicine Dr. Domenico Accili, MD., and Chutima Talchai, PhD., found that when they turned-off Foxol – a gene that plays a big role in determining a cell’s fate –the mouse’s intestine was able to generate insulin-producing cells throughout adulthood.

According to the researchers, the study can provide a lead to a new approach of treating type 1 diabetes in humans. Originally, stem cell transplant was regarded as the ideal way to replace cells lost in type 1 diabetes, as a means of freeing patients from insulin injection. Now, with the mouse research, stem cell transplant does not have to be the only option.

“Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients,” said Dr. Accili.

The researchers originally targeted the progenitor cells in the gastrointestinal tract (GIT) of the mice and tried to discover if they were able to create insulin-producing cel Progenitor cells located in the GIT is generally responsible for creating serotonin, gastric inhibitory peptide and other hormones.

“Nobody would have predicted this result,” said Dr. Accili. “Many things could have happened after we knocked out Foxol. In the pancreas, when we knock out Foxol, nothing happens. So why does somethinghappen in the gut? Why don’t we get a cell that produces some other hormone? We don’t yet know.” Dr. Accili added, “All these findings make us think that coaxing a patient’s gut to make insulin-producing cells would be a better way to treat diabetes than therapies based on embryonic or iPS [induced pluripotent stem] cells.” He said that in order to make the finding into a viable therapy for diabetics, they would have to find a drug that has the same effect on the GIT progenitor.

The key to turning the finding into viable therapy, Dr. Accili says, will be to find a drug that has the same effect as knocking out the Foxol in mice, which is very possible since the researchers were able to create insulin-producing cells from the progenitor cells by using a halting chemical on the Foxol in people as knocking out the Foxol gene does in mice. That should be possible, he says, since the researchers found that they could also create insulin-producing cells from progenitor cells by inhibit Foxol with a chemical.

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