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LDL receptor reduces LDL production, removes cholesterol from blood

MADISON -- A cell membrane protein thought mainly to bind "bad" cholesterol and remove it from circulation also plays a major role in reducing the production of that cholesterol, according to a study published this February in the Journal of Clinical Investigation.

The University of Wisconsin-Madison study provides new insights into the nature of lipoprotein overproduction in people with familial hypercholesterolemia (FH), an inherited disease that affects one in 500 people. The research also explains how statins, a class of medications taken by several million Americans, work to lower blood cholesterol levels.

Low-density lipoprotein (LDL) carries cholesterol to other cells in the body that need it. People whose blood levels of LDL -- the "bad" cholesterol -- are too high have an increased risk of heart disease. Individuals with FH have extremely high levels of LDL and are at high risk for heart attacks at an early age.

"In the 1970s researchers discovered that the LDL receptor is responsible for removing most of the cholesterol from blood," according to Alan Attie, a biochemist in the UW-Madison College of Agricultural and Life Sciences. "They showed that a mutation in the gene that codes for the LDL receptor causes FH. Most people thought that the receptor's major function was to clear LDL from blood."

However, scientists later found that people with FH have high LDL levels not only because they clear it from their blood too slowly, but also because they produce too much, Attie says. "Ours is the first study that explains the paradox of why people with FH produce too much LDL," he says. "We showed that functional LDL receptors increase the degradation of apolipoprotein B inside liver cells."

Apolipoprotein B (apoB) is the major protein component of very low-density lipoprotein, which is made by liver cells and converted to LDL in the blood. The rate of apoB production in liver cells -- and thus LDL production -- is determined by how much a
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Contact: Alan Attie
attie@biochem.wisc.edu
608-262-1372
University of Wisconsin-Madison
4-Apr-2000


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