Triglycerides and cholesterol are essential constituents of the organism. Among other things, triglycerides represent a form of energy store and cholesterol is a basic building block of biological membranes. Both lipids are water insoluble and require appropriate trans
Lipoprotein metabolism. Entero-cytes release absorbed lipids in the form of triglyceride-rich chylomicrons. Bypassing the liver, these enter the circulation mainly via the lymph and are hy-drolyzed by extrahepatic endothelial lipoprotein lipases to liberate fatty acids. The remnant particles move on into liver cells and supply these with cholesterol of dietary origin.
The liver meets the larger part (60%) of its requirement for cholesterol by de novo synthesis from acetylcoen-zyme-A. Synthesis rate is regulated at the step leading from hydroxymethyl-glutaryl CoA (HMG CoA) to mevalonic acid (p. 157A), with HMG CoA reductase as the rate-limiting enzyme.
The liver requires cholesterol for synthesizing VLDL particles and bile acids. Triglyceride-rich VLDL particles are released into the blood and, like the chylomicrons, supply other tissues with fatty acids. Left behind are LDL particles that either return into the liver or supply extrahepatic tissues with cholesterol.
LDL particles carry apolipoprotein B 100, by which they are bound to receptors that mediate uptake of LDL into the port vehicles in the aqueous media of lymph and blood. To this end, small amounts of lipid are coated with a layer of phospholipids, embedded in which are additional proteins—the apolipopro-teins (A). According to the amount and the composition of stored lipids, as well as the type of apolipoprotein, one distinguishes 4 transport forms:
cells, including the hepatocytes (receptor-mediated endocytosis, p. 27).
HDL particles are able to transfer cholesterol from tissue cells to LDL particles. In this way, cholesterol is transported from tissues to the liver.
Hyperlipoproteinemias can be caused genetically (primary h.) or can occur in obesity and metabolic disorders (secondary h). Elevated LDL-cho-lesterol serum concentrations are associated with an increased risk of atherosclerosis, especially when there is a concomitant decline in HDL concentration (increase in LDL:HDL quotient).
Treatment. Various drugs are available that have different mechanisms of action and effects on LDL (cholesterol) and VLDL (triglycerides) (A). Their use is indicated in the therapy of primary hy-perlipoproteinemias. In secondary hy-perlipoproteinemias, the immediate goal should be to lower lipoprotein levels by dietary restriction, treatment of the primary disease, or both.
Drugs (B). Colestyramine and colestipol are nonabsorbable anion-exchange resins. By virtue of binding bile acids, they promote consumption of cholesterol for the synthesis of bile acids; the
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