THURSDAY, Feb. 19 (HealthDayNews) -- You're overweight and have type 2 diabetes. Your doctor urges you to drop those excess pounds, knowing a leaner you will have a better chance of managing your blood sugar.
Today, scientists may be a bit closer to knowing just why that's so.
A new study on mice, published in the Feb. 20 issue of Science, suggests a fat-derived hormone called resistin may promote insulin resistance, a condition in which the body fails to use insulin properly.
Insulin is the substance that controls blood sugar in the body. When there isn't enough of it or it isn't used effectively, sugar builds up in the blood, starving the cells of the fuel they need for energy.
Mice that don't have resistin are largely protected from insulin resistance, says Dr. Mitchell Lazar, director of the
If resistin plays a similar role in humans, the authors say, this finding could lead to new ways to diagnose and treat people with type 2 diabetes.
"We might be able to really make an impact on insulin resistance and, therefore, on diabetes," Lazar says.
About 17 million Americans have type 2 diabetes, according to the American Diabetes Association. The disease frequently goes undiagnosed yet poses serious and life-threatening complications such as blindness, kidney disease, heart disease and stroke.
Carrying extra body fat puts people at increased risk. About 80 percent of adults with type 2 diabetes are overweight, according to the National Diabetes Information Clearinghouse.
Perhaps not surprisingly, the nation's diabetes epidemic tracks a dramatic rise in obesity among adults and children in the
In 2001, Penn scientists first reported the existence of a hormone produced by fat cells that seemed to promote insulin resistance. They christened it "resistin," suggesting resistance to insulin.
In the current study, the Penn team bred mice without resistin and compared their blood sugar regulation with mice possessing the hormone. Both groups of rodents gained weight on a high-fat diet, but glucose tolerance was significantly better in the resistin-free mice. Those lacking resistin also had lower fasting blood glucose levels than normal mice.
Lazar believes resistin may have played an important role in evolution, helping to keep blood sugar normal during periods of fasting. With obesity, he says, resistin may get out of whack and contribute to difficulties handling blood glucose.
Dr. Richard Hellman, medical director of the Heart of America Diabetes Research Foundation, says the study is interesting, particularly in light of a growing body of research examining the function of fat cells and fat metabolism.
"What it doesn't say is how this extrapolates to humans," Hellman observes. Nor does it say how important resistin is within the hierarchy of factors that could be contributing to insulin resistance, he adds.
Translating the results to people becomes tricky, Lazar explains, because resistin in humans is expressed mainly by white blood cells, not fat cells as in mice.
"It may not be coming from fat cells but still may be an important link between obesity and insulin resistance in people," he says.
