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In a major breakthrough with far-reaching implications for diseases ranging from heart disorders to diabetes, researchers Wednesday announced finding a gene for obesity.

The molecular identification of the gene called obese, or ob for short, in the mouse and its human homologue opens the door to new understanding and, potentially, treatment of the disorder affecting millions, said Dr. Jeffrey Fried-man of the Howard Hughes Medical Institute at The Rockefeller University in New York, who headed the research team.Obesity, the most common nutritional disorder in the Western world, afflicts one in three Americans who weigh at least 20 percent more than their ideal weight. The extra pounds exacerbate serious disorders such as hypertension, diabetes, heart disease and some cancers.

"This finding is a major breakthrough because it gives researchers a powerful new tool for understanding the mechanisms that regulate body weight," said Torsten Wiesel, Nobel Prize-winning neurobiologist and president of the university.

"We now anticipate many additional discoveries in the field and, eventually, even the possibility of devising new drug therapies to treat obesity, a serious disease that predisposes people to such potentially life-threatening conditions as diabetes, heart disease and high blood pressure."

Dr. Phillip Gorden, director of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Md., which helped fund the research, called the finding "exciting."

"This major breakthrough gives us a new basis for understanding energy regulation and obesity in people," he said.

Reporting in the British journal Nature, the researchers said they found the mouse gene ob codes for a protein secreted by adipose tissue, which contains 167 amino acids and is thought to regulate fat storage by signaling the brain to suppress appetite when the body's fat stores are sufficient.

When mutated in mice, the gene no longer delivers its appetite suppressing message, and the rodents develop a syndrome that resembles extreme obesity and Type II diabetes in humans.

"It is gratifying to think that the work may form the basis for new and innovative ways to treat human obesity," said Dr. Purnell Choppin, president of the Howard Hughes center.

The findings support the hypothesis that the protein produced by the ob gene functions as part of the endocrine signaling pathway from adipose tissue that messages the hypothalamus - the brain command post for appetite - to regulate the size of the body's fat deposits, Friedman said.

"This hypothesis now needs to be tested using modern methods of molecular biology," he said.