Washington: In what could benefit
humans in the future, scientists claim to have found a way to
significantly reduce atherosclerosis in rodents which doesn`t
involve lowering cholesterol or eliminating any other obesity
Atherosclerosis is the process through which fatty
substances, such as cholesterol and cellular waste products
accumulate in the lining of arteries. Those buildups, called
plaques, reduce blood flow through artery and can contribute
to heart attack, stroke and even gangrene.
In their study, the scientists from Washington
University inhibited atherosclerosis in mice by interfering
with production of a substance called fatty acid synthase, the
`Journal of Biological Chemistry` reported.
This enzyme converts dietary sugars into fatty
acids in the liver, where it plays an important role in energy
metabolism. But fatty acids are involved in atherosclerosis.
"The plaques that clog arteries contain large amounts
of fatty acids. We engineered mice that are unable to make
fatty acid synthase in one of the major cell types that
contribute to plaque formation. On a standard Western diet
high in fat, the mice had less atherosclerosis than their
normal littermates," lead scientist Clay Semenkovich said.
Animals can`t survive without fatty acid synthase,
so mice in this study were able to make the substance in most
of their tissues. They couldn`t manufacture it, however, in
macrophages, a type of white blood cell that surrounds and
kills invading microorganisms, removes dead cells from the
body and stimulates the action of other immune cells.
"With the current epidemic of obesity and diabetes,
people sometimes forget that it`s the blockages in the
arteries that really kill people
"We`ve made progress using statin drugs, for example,
that lower cholesterol and fight plaque buildup, but a lot of
people who take statins still die from cardiovascular disease.
We need better therapies.
"It may be possible, for example, to take macrophages
out of humans, inhibit fatty acid synthase in those cells, and
then infuse the macrophages back into the same person. "From
what we`ve observed in mice, we`ll hypothesize that approach
might prevent or interfere with plaque buildup in people," the