F. Triacylglycerol and cholesteryl ester resynthesis
The mixture of lipids absorbed by the enterocytes migrates to the smooth endoplasmic reticulum (SER) where biosynthesis of complex lipids takes place. The long-chain FA are first converted into their activated form by fatty acyl coenzyme A (CoA) synthetase (thiokinase), as shown in Figure 15.6. Using the fatty acyl CoA derivatives, the 2-MAG absorbed by the enterocytes are converted to TAG through sequential reacylations by two acyltransferases, acyl CoA:monoacylglycerol acyltransferase and acyl CoA:diacylglycerol acyltransferase. Lysophospholipids are reacylated to form phospholipids by a family of acyltransferases, and cholesterol is acylated primarily by acyl CoA:cholesterol acyltransferase (see p. 232). [Note: Virtually all long-chain FA entering the enterocytes are used in this fashion to form TAG, phospholipids, and cholesteryl esters. Short-and medium-chain FA are not converted to their CoA derivatives and are not reesterified to 2-MAG. Instead, they are released into the portal circulation, where they are carried by serum albumin to the liver.]
G. Lipid malabsorption
Lipid malabsorption, resulting in increased lipid (including the fat-soluble vitamins and essential FA, see p. 182) in the feces, a condition known as steatorrhea, can be caused by disturbances in lipid digestion and/or absorption (Fig. 15.7). Such disturbances can result from several conditions, including CF (causing poor digestion) and short bowel syndrome (causing decreased absorption).
The ability of short-and medium-chain FA to be taken up by enterocytes without the aid of mixed micelles has made them important in medical nutrition therapy for individuals with malabsorption disorders.
H. Secretion from enterocytes
The newly resynthesized TAG and cholesteryl esters are very hydrophobic and aggregate in an aqueous environment. Therefore, they must be packaged as particles of lipid droplets surrounded by a thin layer composed of phospholipids, nonesterified cholesterol, and a molecule of the protein apolipoprotein (apo) B-48 (see p. 228). This layer stabilizes the particle and increases its solubility, thereby preventing multiple particles from coalescing. [Note: Microsomal triglyceride transfer protein is essential for the assembly of all TAG-rich apo B–containing particles in the ER (see p. 228).] The lipoprotein particles are released by exocytosis from enterocytes into the lacteals (lymphatic vessels in the villi of the small intestine). The presence of these particles in the lymph after a lipid-rich meal gives it a milky appearance. This lymph is called chyle (as opposed to chyme, the name given to the semifluid mass of partially digested food that passes from the stomach to the duodenum), and the particles are named chylomicrons. Chylomicrons follow the lymphatic system to the thoracic duct and are then conveyed to the left subclavian vein, where they enter the blood. The steps in the production of chylomicrons are summarized in Figure 15.6. [Note: Once released into blood, the nascent (immature) chylomicrons pick up apolipoproteins E and C-II from high-density lipoproteins and mature. (For a more detailed description of chylomicron structure and metabolism, see p. 227.)]
I. Use by the tissues