Yale Bulletin and Calendar

January 28, 2000

Volume 28, Number 18

Scientists identify direct link
between DQ8 gene, diabetes

Yale researchers, for the first time, have shown that a particular gene can cause insulin-dependent, or Type I, diabetes.

The discovery was made when the researchers induced spontaneous diabetes by injecting an animal model with DQ8, a human gene long suspected to be involved in the development of insulin-dependent diabetes.

The results were published Jan. 3 in the Journal of Experimental Medicine and clearly point to DQ8 as a starting place for studies into Type 1 diabetes prevention, according to Dr. Li Wen, assistant professor of internal medicine at the School of Medicine, who specializes in endocrinology.

Although scientists have known for two decades that there is a close association between HLA-DQ8 and insulin-dependent diabetes, "this is the first time it has been shown in a living organism that HLA-DQ8 causes Type I diabetes," says Wen.

"Not only can we now study DQ8 in more detail in a living organism, this is also very important for work in preventing diabetes," says Wen.

Type I diabetes is an autoimmune disease, which means it is caused by an individual's T- lymphocytes acting against the body's own tissues. In this case, the pancreas is attacked and cannot produce insulin so the individual must take insulin to compensate.

In the experiment by Wen's group, transgenic mice were given the HLA-DQ8 gene together with another molecule, B7, which by itself does not cause diabetes. The mice spontaneously developed all of the classic signs of Type I diabetes -- elevated sugar in their urine, abnormally high blood glucose results, increased thirst and obvious weight loss.

The researchers also studied mice with the HLA-DQ6 gene, a gene associated with resistance to diabetes in humans. These mice showed no sign of diabetes. The question that now can be investigated, says Wen, is whether DQ6 has a role in preventing diabetes from developing, a hypothesis that scientists also have proposed in the past.

"The ultimate goal is to find more effective interventions for the disease," she says.

Wen's coauthors on the study were associate research scientist F. Susan Wong in the Department of Immunobiology; research assistants Jie Tang, Ning-Yuan Chen and Martha Altieri in the Department of Internal Medicine; Dr. Richard Flavell, chair of the Department of Immunobiology; and Dr. Robert Sherwin, director of the Yale Diabetes Endocrinology Research Center.

-- By Jacqueline Weaver

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