burden. Obese people are at greater risk of type II diabetes.
A newly discovered protein may help explain why overweight often suffer from type II diabetes. The protein, dubbed resistin is produced by fat cells and appears to maintain the insulin response cells. The discoveries of new proteins often suggest a therapeutic gain, but in an unusual twist, the researchers made their discovery using an already popular class of drugs for patients with diabetes. Scientists say the findings should help explain how and why drugs work so well -. And can lead to more effective treatments for the disease
One of the health hazards of obesity is an increased risk of type II diabetes, also known as diabetes in adults. The disease begins when the body becomes mysteriously unable to respond to insulin, a key hormone that regulates blood sugar after meals. The cells of patients fail to absorb glucose, sending blood glucose levels to dangerous levels. Over the decades, this can lead to a host of complications, including nerve damage, kidney failure and blindness.
Some of the most effective treatments for type II diabetes belong to a known class of drugs thiazolidinediones (TZDs), which improve insulin response in patients. Scientists were intrigued, because the drugs seem to turn on a gene involved in the development of fat cells. Why a drug against diabetes would also increase the production of fat cells was a mystery - and a bit of a paradox, because the fat cells seem to be the cause of diabetes, said endocrinologist Mitchell Lazar of the University of Pennsylvania School of Medicine in Philadelphia. This connection led Lazar to speculate that drugs could shed light on what goes wrong in the first diabetes.
Lazar and colleagues guessed that the drugs could be turning off a gene that interferes with insulin response, so they looked for genes that become less active in the presence of TZD. In tomorrow's issue of Nature , they describe such a gene, which makes an unknown protein. They called resistin protein because it seems to cause insulin resistance.
The researchers found that fat cells in mice produce resistin and excrete into the bloodstream. overweight mice had significantly higher levels of resistin in their blood - and sugar levels in the blood higher - than did healthy mice. Blocking resistin appears to help animals respond more effectively to insulin. The researchers also found a human gene that is similar to resistin mouse. They provide for experiments to determine whether human cells respond in the same way as mouse cells.
The work "is quite an attractive story," says endocrinologist Jeffrey Flier of Beth Israel Deaconess Medical Center in Boston. Why mice and humans have a gene that causes insulin resistance is still a mystery, but Lazar speculates that evolution has favored organisms with "thrifty genes" that help store and use energy efficiently to help them survive lean times. When there is a lot of food, however, these genes can backfire.
Related Sites
the homepage of Mitchell Lazar
NIDDK information about diabetes
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