This UW research could change weight loss drug programs, but the discovery isn't remarkable simply because of its practical applications. It ranks up there because we now have a physiological understanding of weight control, something that has eluded humanity for years.

The new research focuses on the signals the body sends to the brain, an idea that was actually first put forth back in the early 1950s. Those signals are generated in relation to the amount of body fat you have, explains Dr. Michael Schwartz, a UW endocrinologist the based at Seattle's Veterans Administration Medical Center.

"That signal tells the brain whether you need to eat more or less," he says. "If you deplete your fat stores by going on a diet, the signal will tell your brain you need to eat more. You will, and you will gain weight."

This theory works off the "set-point" idea, whereby the hypothalamus portion of the brain locks onto a body weight. A signal then feeds the brain with information, telling you how much you need to eat. The cycle begins: what you consume affects your weight, and your weight affects the signal telling your brain how much to eat. If you reduce your weight, the signal will tell your brain you need to eat more. Current weight-loss schemes--commercial programs, drugs, hypnosis--try to reduce your weight. But if you do that, signals inside you go haywire, and tell you to eat more. This is the biological reason all commercial weight loss programs fail, according to Dr. John Brunzell, a UW medicine professor.

"There is no fooling the set point," Schwartz adds. "If you start starving your body, you are messing with the equation of how weight is maintained. If calories are cut back, your brain is going to notice and tell you to start eating more. A diet like that throws all this out of whack."

Back to the mice. What made the UW research breakthrough particularly exciting was the fact that human beings possess an equivalent of the mouse's "fat" gene. This was the gene altered in lab mice by the research team of Phrmacology Professor G. Stanley McKnight. The gene caused the extra food eaten by the mouse to be disposed as body heat instead of storing it as fat. Though the gene in people can't be eliminated or tinkered with, the possibility exists that the same resistance to dietary fat could be achieved through drugs.

Such a substance would have to be available in oral form, and have no side effects to be medically useful, a prospect McKnight says is definitely within reach in the next 10 years or so. With such a large market out there, you can bet drug companies hungry for profits will engage in a dog-eat-dog competition to develop the wonder drug.

Mutant Mice Defeat High Fat Diet
Genetics Finally Recognized as a Key to Weight Gain
Drugs Not Total Answer to Weight Loss

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