STANFORD, Calif. Investigators combing the genome in the hope of finding genetic variants responsible for triggering early-onset diabetes may be looking in the wrong place, new research at the Stanford University School of Medicine suggests.
Early-onset diabetes, also known as type-1 diabetes, is an autoimmune disease, caused when the immune system attacks and destroys insulin-producing cells in a person's pancreas.
What triggers that immune response apparently has less to do with having a distinct set of gene variants than how the behavior of genes may differ in people with the disease. That is the finding of a study published in the November issue of Clinical Immunology, by Garry Fathman, MD, professor of immunology and rheumatology, and his colleagues.
The paper builds upon the knowledge that particular immune-system-related gene variants confer type-1 diabetes susceptibility. Many people have those genes, but only a fraction actually develop the disease. This has led many investigators to conduct exhaustive searches of the genome for other elusive genes that, when defective, may predispose someone to type-1 diabetes. Fathman suggests they may be on the wrong track.
Fathman explained it this way: "Take a pair of identical twins, with one having type-1 diabetes. Although both have precisely the same genes, roughly half the time the other twin doesn't get the disease." The same holds true for other autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, he added.
The situation, Fathman said, is reminiscent of the 1988 movie "Twins," starring Arnold Schwarzenegger and Danny DeVito. They may have started out identical, but something diverged, somewhere. Fathman set out to find out what it was seven years ago, in what he described, tongue-in cheek, as "an interesting study that started at the dawn of history."
Rather than try to implicate
|Contact: Bruce Goldman|
Stanford University Medical Center