E: 03/29/2001 4:57 pm ET

A Couch Potato's Fantasy -- Eat More, Weigh Less

By Will Dunham

WASHINGTON (Reuters) - The couch potato's ultimate fantasy -- eating more and weighing less without having to exercise regularly -- could become a reality thanks to a ground-breaking discovery about the way the body burns fat, researchers said on Thursday.

Scientists at Baylor College of Medicine in Houston said mice that had been genetically modified to lack a key enzyme involved in fat metabolism ate as much as 40 percent more food than normal mice but weighed 10 to 15 percent less.

The researchers said their findings could pave the way for the development of a drug that would target the same enzyme in the human body, providing weight loss without requiring people to eat less or exercise more.

"This would be great for the couch potatoes -- guys who can sit on the couch, eat the potato (chips), watch the TV, without worrying about having a bigger paunch. So this is what we feel potentially can be done," Dr. Salih Wakil, who led the study, said in an interview.

The findings could offer hope to the millions of Americans and people in other Western countries who are waging a losing battle against the bulge.

"I want to join those mice and sort of eat to my heart's content without putting on more fat," added Wakil, chairman of Baylor's department of biochemistry and molecular biology. "In the western world, this is a very important thing because of the number of obese people. Obesity is climbing, and is becoming very, very serious."

70 MILLION AMERICANS ARE OBESE

At least 70 million Americans are obese, including more than a third of adults and one in five children, experts said. Obesity causes 300,000 premature deaths in the United States a year. Experts blame a lifestyle that includes too many fatty and sugary foods and too little exercise.

Obesity increases the risk of illness and death due to diabetes, stroke, coronary artery disease, and kidney and gallbladder disorders. Diabetes, the seventh-leading cause of death among Americans, rose 33 percent from 1990 and 1998.

In a study published in the journal Science, researchers zeroed in on an enzyme called acetyl-CoA carboxylase 2, or ACC2, seen predominately in skeletal and cardiac muscle. That enzyme and the related enzyme ACC1 are involved in producing a compound vital to the formation of fatty acids in the body and to fat burning.

The researchers created genetically engineered mice that lacked either one or the other of those enzymes.

The mice without ACC1 all died as embryos. But the mice that lacked ACC2 thrived -- appearing normal and happy and reproducing well, the researchers said. They also ate more, weighed less and accumulated less fat than normal mice. In fact, those mice had 50 percent less body fat than normal mice, as they continually burned fatty acids.

"Basically, you do eat more, but that fat is being burned," Wakil said.

He said the mutant mice were putting less of a hormone called leptin in the bloodstream. Leptin, which plays an important role in regulating food intake and body weight, is produced mainly by fat cells and signals nutritional information to the brain. Higher levels of leptin signal the brain to reduce appetite.

"PLAUSIBLE TARGET" FOR AN ANTI-OBESITY DRUG

In an article accompanying the study, Boston scientists Neil Ruderman of BioSquare II and Jeffrey Flier of Beth Israel Deaconess Medical Center said the bodily mechanism involved in the findings was unclear. But they said creating a drug that would inhibit ACC2 in the human body to provide continual fat burning was "a plausible target" for anti-obesity treatment.

Wakil said he envisioned a drug that could be used for weight loss by obese people and to ward off weight gain in others. "If we find a drug that can be used to regulate ACC2 without having some other side effects, I think we've achieved our goal," he said.

A second study published in Science offered more fodder for anti-obesity drug research. Researchers from the Rockefeller University, the Howard Hughes Medical Institute, Princeton University and the University of California at San Diego demonstrated that the parts of the brain that control emotion and thought also may contribute to feelings of hunger.

The researchers employed a novel technique that used a virus tagged with a green-glowing jellyfish protein to visualize the feeding circuit in the brain of a mouse.

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-- Anonymous, March 29, 2001