A Molecular Explanation of Why Burgers Are Bad For You

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A Molecular Explanation of Why Burgers Are Bad For You

Researchers identify cholesterol-forming mechanism

By Ed Edelson HealthDay Reporter

THURSDAY, Jan. 27 (HealthDayNews) -- Researchers say they have

discovered the molecular switch that turns the bad fats in food into

the cholesterol that clogs your arteries.

It is a molecule designated PGC-1 beta, biochemically classified as

a co-activator, and it plays a role in liver metabolism, according

to a report in the Jan. 28 issue of Cell by scientists at Harvard's

Dana-Farber Cancer Institute.

When the saturated fats and trans-fatty acids in meat, whole-milk

dairy products and other foods on cardiologists' crime sheet arrive

at the liver, PGC-1 beta begins a cascade of biochemical signals

that direct liver cells to produce LDL cholesterol, the " bad " kind

that clogs arteries, as well as triglycerides, another family of

artery-blocking substances, the researchers report.

" This gives us a target for drug development, " said study author

Bruce Spiegelman, a professor of cell biology at Harvard Medical

School. " It might be possible to develop agents for people who can't

be treated with current drug regimens. It also is a way to

understand better why some foods have deleterious effects and some

don't. "

Scientists and cardiologists have known for a long time which foods

are bad for people. Study after study has shown that diets rich in

saturated fats and trans fats -- most notoriously, the burger-and-

fries meal so popular in this country -- increase blood levels of

LDL cholesterol, while foods rich in unsaturated fats are associated

with HDL cholesterol, the " good " kind that helps keep arteries clear.

" We knew these saturated and trans-fatty acids had bad effects, "

Spiegelman said. " We had no idea, in molecular terms, what they did

to set up the bad pathways. What we have found is a missing link, a

mechanism by which saturated fats and trans fats can do their dirty

work. "

As an exercise in pure science, the discovery is another example of

the natural selection process that is at the center of

Darwin's theory of evolution, Spiegelman said.

Until recently in human history, PGC-1 beta did no particular harm

to humans because " most of our evolution did not occur in times of

great nutritional abundance, " he explained. " In addition, its bad

effects are mostly felt in older people, after the child-bearing

years, so there has been no selection pressure. "

Now that people are living longer, the evil effects of PGC-1 beta

have become a target of medical practice, Spiegelman said.

Research to develop compounds that block the activity of PGC-1 beta

could provide new cholesterol-lowering treatments, he added.

" I am hopeful that this paper will stimulate interest on the part of

pharmaceutical companies to do that, " he said.

" This is a very important finding that sheds a great deal of light

on the molecular pathways for production of fats, " said Dr.

Krauss, director of atherosclerosis research at the Children's

Hospital Oakland Research Center in California.

Some findings do require follow-up research, Krauss added. For

example, in humans, consumption of fat-rich foods is believed to

suppress the activity of LDL cholesterol receptors on cells, thus

raising LDL cholesterol blood levels. The new study, done in mice,

found increased activity of LDL cholesterol receptors.

" There might be some details that are different between mice and

humans, " Krauss said.

More information

The cholesterol story, good and bad, is outlined by the American

Heart Association.

Copyright © 2002 ScoutNews, LLC. All rights reserved.

SOURCES: Bruce Spiegelman, Ph.D, professor, cell biology, Dana-

Farber Cancer Institute, Boston; Krauss, M.D., director,

atherosclerosis research, Children's Hospital Oakland Research

Center, Oakland, Calif.; Jan. 28, 2005, Cell