Enterocytes Secrete Chylomicrons and Very Low Density Lipoproteins

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The reassembled triglycerides, lecithin, cholesterol, and cholesterol esters are then packaged into lipoproteins and exported from the enterocytes. The intestine produces two major classes of lipoproteins: chylomicrons and very low density lipoproteins (VLDLs). Both are triglyceride-rich lipoproteins with densities less than 1.006 g/mL. Chylomicrons are made exclusively by the small intestine, and their primary function is to transport the large amount of dietary fat absorbed by the small intestine from the enterocytes to the lymph. Chylomicrons are large, spherical lipoproteins with diameters of 80 to 500 nm. They contain less protein and phospholipid than VLDLs and are, therefore, less dense than VLDLs. VLDLs are made continuously by the small intestine during both fasting and feeding, although the liver contributes significantly more VLDLs to the circulation.

Apoproteins—apo A-I, apo A-IV, and apo B—are among the major proteins associated with the production of chylomicrons and VLDLs. Apo B is the only protein that seems to be necessary for the normal formation of intestinal chylomicrons and VLDLs. This protein is made in the small intestine. It has a molecular weight of 250,000 and it is extremely hydrophobic. Apo A-I is involved in a reaction catalyzed by the plasma enzyme lecithin cholesterol acyltransferase (LCAT). Plasma LCAT is responsible for the esterification of cholesterol in the plasma to form cholesterol ester with the fatty acid derived from the 2-position of lecithin. After the chylomicrons and VLDLs enter the plasma, apo A-I is rapidly transferred from chylomicrons and VLDLs to high-density lipoproteins (HDLs). Apo A-I is the major protein present in plasma HDLs. Apo A-IV is made by the small intestine and the liver. Recently, it was shown that apo A-IV, secreted by the small intestine, may be an important factor contributing to anorexia after fat feeding.

Newly synthesized lipoproteins in the smooth ER are transferred to the Golgi apparatus, where they are packaged in vesicles. Chylomicrons and VLDLs are released into the intercellular space by exocytosis (Fig. 27.27). From

Chylomicrons Size

crograph. The nascent chylomicrons in the secretory vesicle (V) are similar in size and morphology to those already present in the intercellular space (IS). (From Sabesin SM, Frase S. Electron microscopic studies of the assembly, intracellular transport, and secretion of chylomicrons by rat intestine. J Lipid Res 1977;18:496-511.)

crograph. The nascent chylomicrons in the secretory vesicle (V) are similar in size and morphology to those already present in the intercellular space (IS). (From Sabesin SM, Frase S. Electron microscopic studies of the assembly, intracellular transport, and secretion of chylomicrons by rat intestine. J Lipid Res 1977;18:496-511.)

there, they are transferred to the central lacteals (the beginnings of lymphatic vessels) by a process that is not well understood. Experimental evidence seems to indicate that the transfer probably occurs mostly by diffusion. Intestinal lipid absorption is associated with a marked increase in lymph flow called the lymphagogic effect of fat feeding. This increase in lymph flow plays an important role in the transfer of lipoproteins from the intercellular spaces to the central lacteal.

Fatty acids can also travel in the blood bound to albumin. While the most of the long-chain fatty acids are transported from the small intestine as triglycerides packaged in chylomicrons and VLDLs, some are transported in the portal blood bound to serum albumin. Most of the medium-chain (8 to 12 carbons) and all of the short-chain fatty acids are transported by the hepatic portal route.

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