Triglycerides, absorption cells

Thus, in summary, it may be concluded that much of the cholesterol synthesized in the intestine is apparently used for local purposes. Under circumstances where there is no triglyceride absorption taking place essentially no newly synthesized sterol of intestinal origin can be detected in the lymphatic outflow from the gut. During active triglyceride absorption, however, the rate of sterol synthesis increases markedly in the intestinal absorptive cells, and a portion of this newly synthesized cholesterol is incorporated into chylomicrons and other intestinal lipoproteins and delivered into the lymph. Thus, both the rate of sterol synthesis by the intestine and the rate of entry of this sterol into the body pools is partially dictated by the rate of triglyceride absorption. 

The relative importance of each of these contributions to pool C is likely to be different in epithelial cells located at different points along the villus-crypt axis. The fact that cholesterol derived from synthesis and from the uptake of LDL is critically important for membrane formation and differentiation is suggested by the finding that 70-80% of total mucosal sterol synthetic activity and LDL transport activity are localized to the immature cells of the lower villus and crypt regions in both the proximal and distal intestine. In the mature absorptive cells of the upper villus in the jejunum, where most sterol absorption takes place, the rate of cholesterol synthesis appears to be suppressed. In the absence of fat absorption, cholesterol newly synthesized in these cells apparently is sloughed into the lumen and not reabsorbed. However, with active triglyceride absorption cholesterol synthesis in these cells is increased and a portion of this sterol appears in the intestinal lymph. Only under this condition does pool B apparently supply sterol for lipoprotein formation. 

Pfluger (1901), put forward the hypothesis that the complete hydrolysis of glycerides by pancreatic lipase was an essential step in triglyceride absorption. The lipolytic theory , was further advanced by Verzar and McDougal (1936), who also demonstrated the hydrotropic action of bile salts, which causes the solubilization of fatty acids and enables them to cross the intestinal barrier. This theory requires also the resynthesis of the triglycerides in the intestinal cells, to... 

Figure 7. Apical cytoplasm of an intestinal absorptive cell 30 min after administration of a corn oil meal. This micrograph illustrates the sequence of events in the reesterification of triglycerides and the formation of SER lipid-containing vesicles. Free fatty acids and monoglycerides passively diffuse across the microvillus border (MV) and enter the SER of the apical cytoplasm. The latter frequently is in continuity with the RER (arrow 1). As the free fatty acids and monoglycerides are converted into triglycerides, the SER dilates and lipid droplets are formed within the SER cistemae (arrow 2). Eventually the SER loses its continuity with the RER (arrow 3), and discrete, lip id-containing vesicles (L) bud off from the SER to lie free in the cytoplasm. Mitochondria (M). x 26,060. Reduced 12% for reproduction.

ApoA-IV is an immunologically distinct apolipoprotein of Mr 46,000 (B22, G28, W7). It has been demonstrated in intestinal epithelial cells from fasting subjects and a marked increase has been shown during lipid absorption (G27). About 10-13% of chylomicron apolipoprotein and 24-30% of intestinal VLDL apolipoprotein is apoA-IV. In fasting plasma, 98% of apoA-IV is in the d> 1.21 g/ml fraction and in lipemic plasma 90% is in this fraction, while 10% is associated with triglyceride-rich lipoproteins (G27). Gel permeation chromatography confirmed that in plasma most apoA-IV is free, unassociated with lipoproteins (B22, G27). 

Q9 Lipid in the diet is present mostly in the form of triglycerides, which are digested by pancreatic lipase to yield fatty acids and monoglycerides bile salts are also required for digestion and absorption of the dietary lipids. Bile salts interact with the fatty acids and monoglycerides in the gut lumen to form micelles, which can be absorbed by the epithelial cells. In the epithelial cell the triglyceride is resynthesized to form droplets, or chylomicrons, which enter the lacteals and are carried by the lymphatic system into the general circulation. 

A supplementation of procyanidins from cocoa significantly decreased plasma or liver cholesterol and triglycerides in rats fed a high cholesterol diet. The capacity of procyanidins to inhibit intestinal absorption of cholesterol appeared to be one of the mechanisms (Osakabe and Yamagishi, 2009). Cocoa procyanidins had sustained benefits to reverse vascular dysfunction in diabetic patients (Balzer et ah, 2008). Such benefits had been attributed to (—)-epicatechin, which is the constituent unit of cocoa procyanidins (Schroeter et ah, 2006). Procyanidins from cacao were found to inhibit growth of human breast cancer and colonic cancer cells (Camesecchi et ah, 2002 Ramljak et ah, 2005). 

The absorption of vitamin E is relatively poor - only some 20% to 40% of a test dose is normally absorbed from the small intestine, in mixed lipid micelles with other dietary lipids. This absorption is enhanced by medium-chain triglycerides and inhibited by polyunsaturated fatty acids, possibly because of chemical interactions between tocopherols and polyunsaturated fatty acids or their peroxidation products in the intestinal lumen. Esters are hydrolyzed in the intestinal lumen hy pancreatic esterase and also by intracellular esterases in the mucosal cells. 

After its absorption into the intestinal mucosal cell, cholesterol, together with triglycerides, phospholipids, and a number of specific apoproteins, is assembled into a large lipoprotein called the chylomicron (see later section on lipoprotein metabolism, exogenous pathway). One apoprotein component known as apolipoprotein (apo) B-48 is vital to the formation of chylomicrons, and in people with a rare deficiency of apo B-48 synthesis, chylomicron formation, and consequently cholesterol and fat absorption, is severely impaired. Chylomicrons enter the lymphatics, which empty into the thoracic duct and eventually enter the systemic venous circulation at the junction of the left subclavian vein and left internal jugular vein. 

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