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Source: Modified from Kritchevsky, D. (1986) Atherosclerosis and nutrition. Nutr. Int. 2, 290-297.

Source: Modified from Kritchevsky, D. (1986) Atherosclerosis and nutrition. Nutr. Int. 2, 290-297.

proportion of triacylglycerols (see Fig. 17-2). Chylomi-crons are synthesized in the ER of epithelial cells that line the small intestine, then move through the lymphatic system and enter the bloodstream via the left subcla-vian vein. The apolipoproteins of chylomicrons include apoB-48 (unique to this class of lipoproteins), apoE, and apoC-II (Table 21-3). ApoC-II activates lipoprotein lipase in the capillaries of adipose, heart, skeletal muscle, and lactating mammary tissues, allowing the release of free fatty acids to these tissues. Chylomicrons thus carry dietary fatty acids to tissues where they will be consumed or stored as fuel (Fig. 21-40). The remnants of chylo-microns (depleted of most of their triacylglycerols but still containing cholesterol, apoE, and apoB-48) move through the bloodstream to the liver. Receptors in the liver bind to the apoE in the chylomicron remnants and mediate their uptake by endocytosis. In the liver, the remnants release their cholesterol and are degraded in lysosomes.

FIGURE 21-40 Lipoproteins and lipid transport. (a) Lipids are transported in the bloodstream as lipoproteins, which exist as several variants that have different functions, different protein and lipid compositions (see Tables 21-2, 21-3), and thus different densities. Dietary lipids are packaged into chylomicrons; much of their tria-cylglycerol content is released by lipoprotein lipase to adipose and muscle tissues during transport through capillaries. Chylomicron remnants (containing largely protein and cholesterol) are taken up by the liver. Endogenous lipids and cholesterol from the liver are delivered to adipose and muscle tissue by VLDL. Extraction of lipid

When the diet contains more fatty acids than are needed immediately as fuel, they are converted to tria-cylglycerols in the liver and packaged with specific apolipoproteins into very-low-density lipoprotein

(VLDL). Excess carbohydrate in the diet can also be converted to triacylglycerols in the liver and exported as VLDLs (Fig. 21-40a). In addition to triacylglycerols, VLDLs contain some cholesterol and cholesteryl esters, as well as apoB-100, apoC-I, apoC-II, apoC-III, and apo-E (Table 21-3). These lipoproteins are transported in the blood from the liver to muscle and adipose tissue, where activation of lipoprotein lipase by apoC-II causes the release of free fatty acids from the VLDL triacylglycerols. Adipocytes take up these fatty acids, reconvert them to triacylglycerols, and store the products in intracellular lipid droplets; myocytes, in contrast, primarily oxidize the fatty acids to supply energy. Most VLDL remnants are removed from the circulation by hepatocytes. The uptake, like that for chylomicrons, is from VLDL (along with loss of some apolipoproteins) gradually converts some of it to LDL, which delivers cholesterol to extrahepatic tissues or returns to the liver. The liver takes up LDL, VLDL remnants, and chylomicron remnants by receptor-mediated endocyto-sis. Excess cholesterol in extrahepatic tissues is transported back to the liver as HDL. In the liver, some cholesterol is converted to bile salts.

(b) Blood plasma samples collected after a fast (left) and after a high-fat meal (right). Chylomicrons produced after a fatty meal give the plasma a milky appearance.

Liver

Intestine

Intestine

Reverse cholesterol transport ■ ■

trnT r

Liver

Reverse cholesterol transport ■ ■

Extrahepatic tissues

Extrahepatic tissues

Chylomicrons

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