By reducing the amount of insulin, subjects stayed lean.
Live lean and prosper. New research
raises the possibility that drugs might be developed to make human fat cells
less sensitive to insulin, allowing people to eat as much as they like and still
stay slim.
The research, done on genetically altered mice at Harvard Medical School in
Boston, blocked sensitivity to fat cells, which allowed the mice to eat what
they wanted and yet remain lean. They also lived longer than mice that weren't
genetically modified.
An estimated 60 million American adults are overweight, and millions more are at
risk to join them.
"Since insulin is needed to help fat cells store fat, these animals had less fat
and were protected against the obesity that occurs with aging or overeating,"
said Dr. C. Ronald Kahn, a professor of medicine and researcher at Harvard's
Joslin Diabetes Center and leader of the study team.
"They were also protected against the metabolic abnormalities associated with
obesity, including Type 2 (insulin resistant) diabetes," Kahn added. The
National Institute of Diabetes and Digestive and Kidney Diseases sponsored the
research.
The study, published last week in the journal Science, worked with a new strain
of mice, called FIRKO mice (fat-specific insulin receptor knockout), ate normal
diets, but had reduced fat mass - 50-to-70 percent less than controls.
And they were protected against obesity and its related metabolic disorders,
including Type 2 diabetes, which leaves too much sugar unprocessed in the blood
and is usually associated with obesity.
Even when the mice were stimulated to overeat, they didn't gain weight. They had
a life span increase of 18 percent, or 134 days, over the control group. The
researchers found that at 30 months of age, when 45 to 54 percent of the control
mice had died, 80 percent of the FIRKO mice were still alive.
Scientists have observed in a number of experiments that eating less seems to
delay aging, perhaps by decreasing metabolism and the related production of
harmful "free-radical" molecules that contribute to aging.
But it has not been clear if diet restriction increased longevity directly or
whether the longevity was because of being lean. Other factors, including
genetics and environmental factors also contribute to life span, but in the
FIRKO mice, the researchers feel the altered insulin signal played a key role.
"If we were able to find a drug to reduce or block insulin action in fat cells
in humans, we might be able to prevent obesity as well as Type 2 diabetes," Kahn
said. "And who knows, they might also live longer."
Source: Diabetes In Control.Com.
January 2003 News Article Index
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