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Food Lipids: Chemistry, Nutrition, and Biotechnology

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70% of the total amount of cholesterol in the plasma. Most of the LDL is now<br />

removed from the circulation through the hepatic LDL receptor pathway, which recognizes<br />

apolipoprotein B-100 (apoB-100). LDL uptake from the blood by the LDL<br />

receptor–mediated pathway is highly controlled <strong>and</strong> this pathway will be downregulated<br />

if the amount of cholesterol in the cell becomes too high. A smaller part,<br />

however, is removed via the scavenger pathway. Uptake via this pathway is not<br />

saturable <strong>and</strong> is positively related with the LDL cholesterol concentration. Thus, the<br />

higher the blood LDL cholesterol concentration, the more LDL will be taken up via<br />

the scavenger pathway [1]. When too much LDL is taken up via the scavenger<br />

pathway from macrophages, cells loaded with cholesterol are formed—so-called<br />

foam cells—which are frequently found in atherosclerotic lesions.<br />

Cholesterol can also be transported out of tissues by reverse cholesterol transport.<br />

This system is mediated by HDL, lecithin cholesteryl acyltransferase (LCAT)<br />

<strong>and</strong> cholesterol ester transfer protein (CETP). HDL binds free cholesterol from tissues,<br />

which is esterified by LCAT, a protein associated with apolipoprotein A-I<br />

(apoA-I). The formed cholesterylesters move to the core of the HDL particle <strong>and</strong> the<br />

HDL is converted to a larger particle. The acquired cholesterylesters can now be<br />

transferred with the assistance of CETP to apoB-100-containing lipoproteins in<br />

exchange for triacylglycerols. The apoB-100-containing lipoproteins are further metabolized,<br />

as has already been described. The large HDL particles may also be taken<br />

up in the liver by a putative HDL receptor or lose a part of its content by the action<br />

of hepatic lipase <strong>and</strong> then reenter the circulation again.<br />

V. PLASMA LIPOPROTEINS AND CORONARY HEART DISEASE<br />

LDL <strong>and</strong> HDL have different effects on the risk for CHD. High concentrations of<br />

LDL are atherogenic, whereas high levels of HDL are negatively associated with the<br />

risk for CHD. As LDL carries most of the plasma cholesterol, the total plasma<br />

cholesterol is also a good index for the risk of CHD. It should be realized, however,<br />

that some people have high total cholesterol concentrations, due to high HDL levels.<br />

Therefore, the total cholesterol to HDL cholesterol might be the most efficient predictor<br />

for the risk for CHD [2]. Also, high levels of triacylglycerols, which are in<br />

the fasting condition mainly found in the VLDLs, are positively related to the risk<br />

for CHD [3].<br />

VI. DIETARY FATS AND PLASMA LIPOPROTEINS<br />

A. Earlier Studies<br />

In the 1950s Keys <strong>and</strong> coworkers started a series of well-controlled experiments to<br />

examine the effects of dietary fatty acids on plasma total cholesterol concentrations<br />

[4,5]. Groups of physically healthy men were fed diets that differed widely in the<br />

amount of fat <strong>and</strong> in dietary fatty acid composition. During the studies, individual<br />

allowances were adjusted weekly to keep body weight stable so that changes in<br />

plasma total cholesterol concentrations could be attributed solely to dietary changes.<br />

At the end of the studies, an empirical formula was derived that could be used to<br />

predict for a group of subjects changes in plasma cholesterol concentrations from<br />

changes in dietary fatty acid composition:<br />

Copyright 2002 by Marcel Dekker, Inc. All Rights Reserved.

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