(LOS ANGELES December 29, 2003) For over a decade, scientists have known that insulin resistance a syndrome where the body does not respond as well as it should to insulin is linked to the development of heart disease, diabetes, high blood pressure, obesity and polycystic ovary syndrome. In fact, one in four adult Americans has insulin resistance, with Mexican Americans having the highest prevalence. But because people with insulin resistance are so likely to develop diseases such as diabetes and heart disease, scientists have turned their attention on investigating whether a common gene abnormality may be involved.

Now, researchers at Cedars-Sinai Medical Center, in collaboration with investigators at UCLA, have found that lipoprotein lipase (LPL), a gene that controls the delivery of fatty acids to muscle and tissues in the body, is linked to insulin resistance in Mexican-Americans. Their findings, reported in the January issue of Diabetes, may enable scientists to design therapies that target LPL to prevent insulin resistance, a condition estimated to affect over 80 percent of the 16 million Americans with Type 2 diabetes, and additional millions at risk for heart disease.

"This is the first study to definitively show that LPL is a gene for common insulin resistance," said Jerome I. Rotter, M.D., Director of the Division of Medical Genetics and Director of the Common Disease Genetics Program at Cedars-Sinai Medical Center.

In recent years, LPL has emerged as a likely "gene candidate" to study for insulin resistance because some studies had linked it to high blood pressure, obesity, and atherosclerosis (fatty deposits in the arteries) all of which are associated with the insulin resistance syndrome. But the studies were small, used limited diagnostic tests, and looked at only small portions of the LPL gene.

To determine whether LPL was directly linked to insulin resistance, researchers under Dr. Rotter's direc
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Contact: Kelli Hanley or Sandy Van
kelli.hanley@cshs.org
310-423-3674
Cedars-Sinai Medical Center
29-Dec-2003

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