Report Explores Cause of Diabetes

By David Brown
Washington Post Staff Writer
Monday, January 16, 2006

A team of Icelandic researchers has identified a gene that may play a part in up to one-fifth of the cases of Type 2 diabetes in the United States.

The gene's function is not known for certain but it appears to play a role in the regulation of other genes involved in hormone secretion.

The discovery was made by scientists at a Reykjavik company called DeCode Genetics Inc., which seeks the genetic underpinnings of disease using Iceland's population as a research tool.

Iceland is a fruitful place for such work because the population is small and ethnically homogeneous, and has extremely good medical records. The findings were published online yesterday in the journal Nature Genetics.

With diabetes, the body cannot adequately regulate glucose, its main fuel.

In Type 1 diabetes, the body does not make enough insulin, the hormone that helps move sugar molecules from the bloodstream into cells. In Type 2 the body makes insulin, but cells resist its action. About 90 percent of diabetes cases are Type 2, with overweight people at increased risk.

Chronically high levels of bloodstream sugar can lead to myriad complications, including kidney failure, blindness and nerve and blood-vessel damage.

The team, led by Struan F.A. Grant and Kari Stefansson, looked at a large number of genetic "markers" in 1,185 Icelanders with Type 2 diabetes and 931 without.

They found a gene that has several variations -- one that offers partial protection against diabetes and two that increase a person's risk for the disease.

In the Icelanders, 33 percent of diabetics had one of the "risky" variations of the gene, whereas only 26 percent of people without diabetes had one. In a sample of mostly white Americans, the split was 39 percent and 25 percent.

Using an estimate of how common the gene variations are in three populations -- Icelanders, Danes and white Americans -- the researchers calculated that about 21 percent of Type 2 diabetes could be attributed to the presence of the "risky" variations.

The gene, called TCF7L2, is not an all-or-nothing predictor of diabetes risk. It is likely that people carrying its deleterious versions could counteract the risk through measures such as controlling weight and increasing exercise.

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