After 20 weeks on the diets, the mice that had the active ACAT2 enzyme and were fed saturated fat and both types of monounsaturated fat had higher levels of cholesterol and more atherosclerosis than the mice that were fed polyunsaturated fats.

All of the mice without the ACAT2 enzyme were protected against atherosclerosis, which is the buildup of fatty deposits in the blood vessels that can lead to heart attacks and strokes.

"Regardless of the diet fed, the mice without ACAT2 were protected from atherosclerosis," said Rudel.

Eliminating ACAT2 did not interfere with the normal processing of cholesterol. ACAT2 is one of three enzymes that can change cholesterol into a form that can be more easily carried in blood. Studies in both mice and monkeys show that when cholesterol is altered by ACAT2, it is more likely to build up in blood vessel walls and cause atherosclerosis.

Rudel hopes to get funding to repeat the study in monkeys.

"If it works in monkeys, it would be proof of concept that it could work in humans," he said.

He also hopes the research will lead to a drug that can inhibit the enzymes actions in humans. Currently, there is a compound that can block ACAT2, but it must be injected so isnt quite as practical as a drug. He is collaborating with a pharmaceutical company that is working to find a compound that could be taken orally.

Scientists already know that humans produce ACAT2 in the liver and that women have lower levels than men. Research has shown that estrogen can lower ACAT2 production, which may partly explain why women are less likely than men to get heart disease during their estrogen-producing years.

"All of these findings tell us that a potential treatment for protecting against heart disease is a compound that decreases ACAT2 activity," said Rudel.

The findings are reported online by Arteriosclerosis, Thrombosis and Va
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