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Cellular fat sensor slows heart disease

A cellular sensor of dietary fats slows the development of lesions that lead to heart disease, a Salk Institute study has found.

The study, which appears in the Oct. 17 edition of Science and is posted on the journal's web site, uncovers a unique pathway that significantly curbs the development of atherosclerosis - the accumulation of fatty deposits on arterial walls. The pathway could be used to develop drugs to treat heart disease, currently the number one killer of Americans.

Ronald Evans, the March of Dimes Chair in Molecular and Developmental Biology at the Salk Institute, research fellow Chih-Hao Lee and colleagues found that the regulatory molecule, PPAR-delta (short for peroxisome proliferator-activated receptor), plays a powerful part in the body's inflammatory response to the beginning phases of atherosclerosis.

"Immune cells promote inflammation, which stimulates the transport and absorption of fat that triggers the early stages of heart disease," Evans said. "Our study uncovered the molecular switch that regulates this process and reveals how the inflammatory response, designed to fend off invading agents, can go awry and encourage atherosclerosis and heart disease."

The researchers found that the PPAR-delta switch cut heart disease in half. It does this by disrupting a cellular signal that controls the inflammatory response.

Activation of PPAR-delta by a fat-like drug reduces inflammation and discourages the growth of atherosclerotic plaques.

"The lesions that cause atherosclerosis are very complex, and are aggravated," said Evans. "We believe that PPAR-delta normally acts as a molecular soldier to guard against inflammation and disease. Unfortunately, these good effects are compromised by high fat diets, poor exercise, infections and stress. Chemicals that regulate the activity of PPAR-delta could form the basis of a new drug to reduce atherosclerosis and therefore be a possible therapy for heart diseas
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Contact: Andrew Porterfield
porterfield@salk.edu
858-453-4100 ex 1340
Salk Institute
16-Oct-2003


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