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Researchers Use Gene to End High Blood Sugar in Mice

Whether method might someday help people awaits further study

WEDNESDAY, March 18 (HealthDay News) -- Delivering a gene called neurogenin3 into the livers of diabetic mice activates adult stem cells that promote steady insulin production, say researchers at the Baylor College of Medicine in Houston.

The mice had type 1 diabetes. Within a week after the gene was delivered using a disarmed virus, the researchers said, the rodents' blood sugar levels returned to normal and remained that way for the rest of their lives.

The gene triggers a two-step response. First, neurogenin3 goes into the mature liver cells and causes them to make small quantities of insulin, enough to reduce blood sugar levels to normal.

"This is a transient effect. Liver cells lose the capacity to make insulin after about six weeks," Dr. Vijay Yechoor, assistant professor of medicine-endocrinology at Baylor and the study's first author, said in a news release from the college.

Other cells that make larger amounts of insulin show up later. These cluster around the portal veins, which carry blood from the intestines and abdominal organs to the liver. These new cells, which look similar to pancreatic islet cells that normally make insulin, come from a small population of adult stem cells usually found near the portal vein, the authors said.

These stem cells normally act as reserves in case of liver injury. When the liver is damaged, the stem cells form mature liver cells or bile duct cells. But neurogenin3 changes their programming so that they become insulin-producing beta cells in the liver, the researchers said.

The study appears in the March issue of Developmental Cell.

Though the finding is important, much more research is needed before similar results might be seen in humans, Yechoor and his colleagues said.

More information

The U.S. National Diabetes Information Clearinghouse has more about diabetes.

-- Robert Preidt

SOURCE: Baylor College of Medicine, news release, March 16, 2009

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