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Absorption and Metabolism of Lipid in Humans

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Absorption and Metabolism of Lipid in Humans Lipids in Modern Nutrition, edited by M. Horisberger and U. Bracco. Nestle Nutrition, Vevey/Raven Press, New York © 1987. Absorption and Metabolism of Lipid in Humans Patrick Tso and Stuart W. Weidman Departments of Physiology and Medicine, The University of Tennessee Center for the Health Sciences, Memphis, Tennessee 38163 DIETARY LIPIDS Dietary lipids can provide as much as 40% of the daily caloric intake in the Western diet. The daily dietary intake of lipid by humans in the Western world ranges between 60 and 100 g (1,2). Triglyceride (TG) is the major dietary fat in humans. Long-chain fatty acids such as the oleate (18:1) and palmitate (16:0) are the major fatty acids (FA) present. In most infant diets, fat becomes a major en- ergy source. In human milk and in human formulas, 40% to 50% of the total calo- ries are present as fat (3). The human small intestine is presented daily with other lipids such as phospholipid (PL) and cholesterol and other sterols. Both PL and cholesterol are major constituents of bile. In humans, the biliary PL is a major contributor of the luminal PL. It has been calculated that 11 to 12 g of biliary PL enters the small intestinal lumen daily, whereas the dietary contribution is 1 to 2 g (4). The predominant sterol in the Western diet is cholesterol. However, plant sterols account for 20% to 25% of total dietary sterol (5-7). It is beyond the scope of this review to discuss the absorption of lipid soluble vitamins, and the interested readers should refer to the excellent review by Barrowman (8). INTRALUMINAL DIGESTION OF LIPIDS Although the majority of the digestion of TG occurs in the small intestine, the digestion starts in the stomach. Lipase activity has been reported to be present in the human gastric juice (9). This lingual lipase is derived from a group of serous glands (Von Ebner) beneath the circumvallate papillae (3). The lingual lipase plays a particularly important role in the digestion of milk TG, and this compensates for the low pancreatic activity in the newborn. Readers interested in the subject of lingual lipase should refer to the review by Hamosh (3). Lipid emulsion enters the small intestinal lumen as fine lipid droplets less than 0.5 (i-m in diameter (10,11). The combined action of the bile and the pancreatic juice brings about a marked 2 UPID ABSORPTION AND METABOUSM IN HUMANS change in the chemical and physical form of the ingested lipid emulsion. The di- gestion of TG is brought about by the pancreatic lipase in the upper part of the intestinal lumen. The pancreatic lipase works at the interface between the oil and the aqueous phases. The velocity of lipolysis depends on factors modifying the physicochemical properties of the interface as well as the surface area (12-15). Pancreatic lipase acts predominantly at the 1- and 3-ester bonds of TG to release 2-monoglyceride (MG) and free FA (13,16-18). Through isomerization, the 2-MG can be converted to 1-MG. However, this reaction probably occurs slowly in the intestine (19). A pancreatic esterase has been demonstrated by Hofmann and Borg- strom (20) that catalyzes the hydrolysis of 1- or 2-MG to form glycerol and FA. The pancreatic esterase works more efficiently with the 1-isomer than with the 2- isomer. In vitro studies using purified pancreatic lipase have demonstrated a potent in- hibitory effect of bile salts on lipolysis of TG at concentration above critical micel- lar concentration (21,22). The inhibitory effect of bile salt is physiological as the concentration of bile salts in the duodenum is normally higher than the concentra- tion of bile salt needed to observe the inhibitory effect. The pancreas synthesizes another protein that antagonizes the inhibitory action of bile salts. This factor was first isolated by Morgan et al. (23) from rat pancreatic juice. The structure and action of colipase have predominantly been elucidated by the work of Desnuelle and his group in Marseille, and Borgstrom and co-workers in Lund (22,24,25). Colipase acts by attaching to the ester bond region of the TG molecule. In turn, the lipase binds strongly to the colipase by electrostatic interactions, thereby allow- ing the hydrolysis of the TG by the lipase molecule (26). Colipase is secreted as a procolipase and is converted to the active form through trypsin digestion (27). The majority of luminal PL is phosphatidylcholine (PC). Both biliary and di- etary PC are hydrolyzed in the presence of pancreatic phospholipase A2 to form lysophosphatidylcholine (LPC) and FA (28,29). Although it is generally accepted that bile PC or dietary PC is only absorbed after hydrolysis by pancreatic phospho- lipase A2 to form 1-lysophosphatidylcholine (28,30,31), it has been proposed that biliary PC is resistant to the action of phospholipase A2, there being an enterohe- patic circulation of bile PC (32-34). This hypothesis needs to be further investi- gated. Cholesterol ester entering the small intestinal lumen is hydrolyzed in the presence of the pancreatic cholesterol esterase to form free sterol prior to its ab- sorption (35,36). UPTAKE OF DIGESTED FAT BY THE ENTEROCYTE The lipolytic products distribute themselves between the aqueous and the oil phases. In the aqueous phase, the lipolytic products exist mainly as part of the mixed bile salt micelle, although some exist in very low concentrations as mono- molecular species in classical solution. This complex problem has been ably re- viewed by Hofmann (37). As digestion progresses, the oil phase gets smaller in volume because of the lipolytic products passing into the mixed micelles and into LIP1D ABSORPTION AND METABOLISM IN HUMANS 3 the absorptive cells. This concept has recently been challenged by the findings of Carey and associates (38-40). They demonstrated the presence of two dispersed phases within the aqueous phase, a phase of micelles saturated with lipids and cho- lesterol (hydrodynamic radii, 200 A) and a phase of unilamellar vesicles (lipo- somes) with radii of 400 to 600 A saturated with bile salts (11). The unilamellar vesicles of mixed lipids saturated with bile salts may play an important role in the uptake of lipid in bile-salt deficient patients (11,41). Further experiments are needed to elucidate the physiological importance of Carey and co-workers' obser- vation. There is a consensus that the uptake of lipid digestion products is passive (42,43). Micellar solubilization increases uptake of the lipid digestion products by increasing their aqueous concentration gradient across the unstirred water layer (42,44-46). How the unstirred water layer affects lipid uptake is complex. The subject has been thoroughly reviewed by Thomson and Dietschy (43). The lipid digestion products enter the enterocytes as monomers (44,47). There are still a few interesting observations for which we do not have an explanation. First, why is p- sitosterol so poorly absorbed relative to cholesterol? The uptake of cholesterol by the enterocytes is different from that of the other lipid digestion products. The ab- sorption of cholesterol seems to involve the collision of the micelle with the brush border membrane, and the disruption of the micelle as a result of monoglyceride and FA absorption might enhance the entry of cholesterol into the lipid membrane (48). In in vivo experiments, the cholesterol was absorbed much more efficiently than the p-sitosterol. However, this selectivity was lost in in vitro experiments. Thus, this membrane selectivity may be energy dependent. Sylven (49), by oc- cluding the blood supply to the jejunum, markedly reduced sterol uptake in the otherwise intact animal, thus supporting the theory that this membrane discrimina- tion of sterol absorption is energy dependent. Secondly, is the unstirred water layer physiologically very important? If so, how are patients with bile salt defi- ciency able to absorb lipid so well? METABOLISM OF ABSORBED LIPID DIGESTION PRODUCTS Once the lipid digestion products enter the cell, the major site of their metabo- lism is at the endoplasmic reticulum (50,51). The mode of transport of these diges- tion products is presumably by simple diffusion. A fatty acid binding protein (FABP) has been described and characterized (52,53). Ockner and Manning (53) suggested a possible role of FABP in regulating TG biosynthesis by adjusting the amount of FA made available for activation and incorporation into TG. The absorbed 2-MG and FA are reconstituted into TG through the monoglycer- ide pathway. The enzymes involved exist as an enzyme complex called the "tri- glyceride synthetase" (54). The other pathway for the synthesis of TG from the absorbed FA is the a-glycerophosphate pathway. The a-glycerophosphate path- way is particularly important under conditions where the supply of FA is far more 4 UPID ABSORPTION AND METABOLISM IN HUMANS abundant than the MG. When MG and FA are absorbed together, the MG pathway plays a more important role than the a-glycerophosphate pathway. This is sup- ported by data both in animals (17,55) and also in humans (56). The reasons why the MG pathway is the preferred pathway are three-fold. First, the MG pathway has a Km of approximately one-hundredth that of the a-glycerophosphate pathway (57), and, thus, the rate is much faster with the former. Second, it has been sug- gested that the MG pathway may be preferentially activated by bile salts (58). Third, the presence of MG inhibits the a-glycerophosphate pathway and thus fa- vors the MG pathway (59). While TG is the major product of the two pathways, the diglyceride (DG) and the TG originated from these pathways seem to enter different metabolic pools.
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