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Obesity Gene: Possible Link To Heart Disease Risk

DALLAS, June 12 -- A link has been found between leptin, a protein product of the obesity gene, and risk for coronary heart disease, the cause of heart attacks, say researchers in a study published today in an American Heart Association journal.

The obesity gene was cloned in 1994. Its product, leptin, acts as a signal to help the body decide when it has eaten enough food to feel full. The amount of leptin in the blood has been directly linked to body fat.

This study is the first to associate leptin elevations in the blood with so-called insulin resistance syndrome. The syndrome -- characterized by high blood pressure, low levels of the "good" high-density lipoprotein cholesterol and elevations in insulin -- sets the stage for heart disease. Insulin is a hormone that helps the body use glucose, its main fuel. An excess of insulin (a condition called insulin resistance) indicates the body is not processing glucose normally.

The study was conducted by researchers in the Wynn department of metabolic medicine of the Imperial College School of Medicine, London.

In the study, which appears in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association, researchers measured blood leptin levels in 74 men. They found that the higher the level of leptin the more likely the men were to have the syndrome, and thus "perhaps a greater heart disease risk," says Francisco Leyva, M.D., specialist registrar in cardiology at Charing Cross Hospital.

"We have found that leptin concentrations are related to the metabolic disturbances that constitute the syndrome, especially insulin resistance," says Leyva. "Futher studies are needed to determine whether insulin and leptin play a coordinating role in this syndrome and whether leptin concentrations could provide an additional measure of heart risk.

"Measuring leptin might become a new way to determine a person's risk of heart dis
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Contact: Carole Bullock
caroleb@amhrt.org
214-706-1279
American Heart Association
11-Jun-1998


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