Brain Research Bulletin, Vol. 21, PP. 411482.
0361-9230/91 $3.00 + .OO
0 Peqaraon Press plc, 1991. Printed in the U.S.A
The Absorption and Transport of Lipids by the Small Intestine PATRICK
TSO” AND KAZUMA
FUJIMOTO
Department of Physiology, Louisiana State University Medical Center, Shreveport, LA 71130
TSO, P. AND K. FUJIMOTO. The absorption and transport of lipids by the small infestine. BRAIN RES BULL 27(3/4) 477482, 1991. -Dietary lipid provides as much as 40% of the caloric intake in the Western diet. Triacylgiycerol is the main dietary fat. The human small intestine is also presented daily with II-12 g of phosphol~pid, predominantly phosphatidyicholine. The predominant sterol in the Western diet is cholesterol, which is derived from animal fat. Plant sterols account for up to 20-25% of total dietary sterol. This paper reviews our current unde~t~ding of the process and the factors that regulate the absorption and
transport of different dietary lipids by the human small intestine. Intestinal lipid absorption
Intestinal lipid metabolism
hydrolyzed to form predomin~tly 2-monoglyceride (MG) and fatty acid (FA) (6,ll). Experiments in vitro have demonstrated that the lipolytic action of lipase on a lipid emulsion containing TG and bile salts occurs slowly, resulting from the inhibition caused by bile salts at concentrations above critical micellar concentration (8). However, inhibition can be overcome by another protein in pancreatic juice called colipase (8). In the newborn, the pancreatic lipase system is not fully developed, and gastric lipase plays an important role in the digestion of milk fat. Readers interested in the subject of gastric lipase should refer to the review by Hamosh (22). Luminal PC is digested in the presence of pancreatic phospholipase A2 to form lysophosphatidylcholine (LPC) and fatty acid (FA) (34,43). Cholesterol can only be absorbed by the small intestine in the free form. Thus, dietary cholesteryl ester has to be hydrolyzed by cholesterol esterase (10) to form free cholesterol prior to absorption by the enterocytes.
NUMEROUS reviews have been written on the digestion and absorption of lipid by the small intestine (50,5 1). In this review, we will summarize our current understanding of how dietary lipid is digested and taken up by the epithelial cells (enterocytes) of the small intestine and of the factors regulating the intestinal formation and release of chylomicrons (CM) and very low-density lipoproteins (VLDL). DIETARY LIPIDS
As much as 40% of the daily caloric intake in the Western diet is in the form of lipids. Triacylglycerol (TG) is the major form of dietary fat in human beings and each glycerol backbone is esterified with three fatty acids (FA), mostly long-chain FA. common long-chain FA are palmitate (C 16:0), stearate (18:0), oleate (C l&l, w9), and linoleate (C 18:2, ~6). Because of the beneficial health effects associated with eating fish, there has been an increased consumption of fish or fish oil products. These benefits are related to the two major omega-3 FA present, eicosapentaenoate (C 205, ~3) and docosahexaenoate (C 22:6, ~3). In human milk formulas, 40-50% of the total calories are present as fat (22). The human small intestine is also presented daily with both dietary and endogenous phosp~olipids and sterols. Of the luminal phospholipids, phosphatidylcholine (PC) is by far the most important. Luminal PC can be derived from both the diet and from bile, but the biliary contribution (11-12 grams per day) (7,5.5) is significantly more than the dietary (l-2 grams per day) (7&S). The predominant sterol in the Western diet is cholesterol. However, plant sterols account for 20-25% of the total dietary sterol (51).
UPTAKE OF LIPID DIGESTION PRODUCTS BY THE ENTEROCYTE
Until very recently, it was generally believed that FA and MG are absorbed by the enterocytes through simple diffusion (50). However, the FA and MG have to overcome the diffusion barrier afforded by the “unstirred water layer” (59). This is achieved by the micellar solubilization of MG and FA by bile salts. Through micellar solubilization, the concentration of FA and MG next to the enterocyte membrane increases markedly, thus facili~ting the entry of these lipids into the enterocytes. MG and FA enter the enterocytes as monomers (50). Recent studies by Stremmel have indicated that there is a FA-binding protein associated with the brush-border membrane, and that this protein seems to play a role in the uptake of FA by enterocytes (47). While the data from Stremmel are certainly convincing, the
DIGESTION OF DIETARY LIPIDS
The bulk of TG digestion occurs in the duodenum of the small intestine. Through the action of pancreatic lipase, TG is -Kequests Ior reprints Should be 71130.
addressedto Dr. Patrick Tso, Department of Physiology,
477
L.S.U.
Med. Ctr., 1501 Kings Highway, Shreveport, LA
478
TSO AND FUJIMOTO
MONOACYLGLYCEROL
PATHWAY
1
0-Z-R
2 0 O-C-R
3 t 1
OH
2
OH
3t
-R._*
2
Phosphahdate Phosphohydrolase
opo,
3
Q
1 GLYCEROL
- 3 - PHOSPHATE
PATHWAY
2
c
.jt FIG.
I. Pathways of triacylglycerol biosynthesis
O-C-R 0 O-C-R
OPO-x
in the rat and hamster intestinal mucosa [adapted from (3O)l.
issue of whether FA is taken up by passive diffusion or by a carrier-mediated process warrants further investigation. Bergstedt et al. (5) have recently demonstrated that stearate seems to be taken up by the small intestine more slowly than oleate. It would be important to compare, both in vitro and in vivo, the uptake of long-chain FA by the small intestine. The uptake of LPC is believed to be passive. However, Stremmel has demonstrated that the brush-border membrane FA-binding protein also has the capacity to bind and transport LPC, thus raising the possibility that LPC transport may also be carriermediated. Uptake of cholesterol by the enterocytes is specific since B-sitosterol (a plant sterol), a molecule that bears considerable resemblance to cholesterol, is poorly absorbed. This specificity requires energy, as the deprivation of blood supply results in free permeability of different sterols (49). INTRACELLULAR METABOLISM OF ABSORBED LIPID DIGESTION PRODUCTS
As yet we do not know how the various absorbed lipids migrate from the site of absorption to the endoplasmic reticulum (ER) where biosynthesis of complex lipids takes place. A fatty acid binding protein present in the small intestine has been isolated and characterized by Ockner and Manning (35) which may play an important role in the intracellular transport of the absorbed FA. Nonetheless, we are still left with the question of how the other absorbed lipids, e.g., monoacylglycerol, get to the ER. Two sterol carrier proteins have been isolated and characterized (41,46), SCP-1 (47,000 mol.wt.) and SCP-2 (13,500 mol.wt.). SCP-1 is important in the microsomal conversion of squalene to lanosterol (46) and SCP-2 participates in the microsomal conversion of lanosterol to cholesterol (41). Although it has been suggested by some investigators that SCP-2 is also
the fatty acid binding protein, recent evidence by Scallen and co-workers (41) strongly indicates that these two are distinct proteins. Studies by Kharroubi et al. (29) have indicated that the SCP-2 isolated from intestinal epithelial cells is identical to the SCP-2 isolated from liver cytosol. As it does in other tissues, SCP-2 presumably plays an important role in the esterification of cholesterol to form ester and also in intracellular transport. 2-MG and FA are reconstituted to form TG mainly via the monoacylglycerol pathway. As shown in Fig. 1, 2-MG is reacylated into TG by the consecutive action of monoacylglycerol acyl transferase and diacylglycerol acyltransferase (27,30). The enzymes involved in this monoacylglycerol pathway are present in a complex called “triglyceride synthetase” (27). A number of studies have demonstrated that the enzymes involved in the MG pathway are located on the cytoplasmic surface of the ER (2). This finding has an important bearing on our understanding of the intracellular packaging of lipoproteins. The data would seem to indicate that TG is formed at the cytoplasmic surface of the ER and that somehow this TG gains entry into the cistemae of the ER. Based on the fact that TG has a low solubility in phospholipid bilayers (3 mol%), Small (45) postulated that TG molecules saturate the membrane rapidly. Once the solubility of TG is exceeded, Small suggests that TG splits the bilayer and forms a small lens that, as it grows, it bulges into either the cytoplasmic side or the cistemal side of the ER. He then suggests that this protrusion pinches off the membrane and forms either lipid droplets in the cytoplasm or precursors of lipoproteins in the cistemae of the ER. Small’s hypothesis has not been demonstrated experimentally. The other pathway present for the formation of TG in the intestinal mucosa is called the cr-glycerophosphate pathway (27,30). As shown in Fig. 1, this pathway involves the stepwise acyla-
INTESTINAL
479
LIPID ABSORPTION
tion of glycerol-3-phosphate to form phosphatidic acid. In the presence of phosphatidate phosphohydrolase, phosphatidic acid is hydrolyzed to form diacylglycerol (DG), which is then converted to TG. The relative importance of the MG pathway and the a-glycerophosphate pathway depends on the supply of 2-MG and FA. During normal lipid absorption, the 2-MG pathway is by far more important because of the extremely efficient conversion of 2-MG and FA to form TG and also because 2-MG inhibits the a-glycerophosphate pathway (27,30). However, when the supply of 2-MG is lacking or insufficient, the a-glycerophosphate pathway becomes the major pathway for the formation of TG. Some of the absorbed LPC is reacylated to form PC (34,43) and remainder is hydrolyzed to form glycero-3-phosphorylcholine (7,55). The liberated FA can be used for TG synthesis, while the glycerol-3-phyosphorylcholine can be readily transported via the portal blood for use in the liver (55). Cholesterol is transported almost exclusively by the lymphatic system, mainly as esterified cholesterol (CE). The rate of esterification of cholesterol may regulate the rate of lymphatic transport of cholesterol. Two enzymes have been proposed to be involved in the esterification, cholesterol esterase (4, 18, 56) and acyl-CoA cholesterol acyltransferase (ACAT) (4,25). Using immunocytochemistry, Gallo et al. (19) have demonstrated that intracellular cholesterol esterase is derived from pancreatic cholesterol esterase (19). A later study by Field (17) confirmed the presence of a cholesterol esterase in the enterocyte. It remains unclear how pancreatic cholesterol esterase is taken up by the enterocyte. There is a lack of general agreement on the relative importance of the two enzymes in the esterification of cholesterol by the enterocytes (4, 18, 56). Furthermore, the relative importance of the two enzymes in the esterification of cholesterol may depend on the exogenous cholesterol load (4). INTRACELLULAR
ASSEMBLY
OF LIPOPROTEINS
As we discussed earlier, the lipid droplet enters the cistemae of the ER. Through a mechanism as yet not well understood, the lipid droplet becomes associated with phospholipids and apolipoproteins. The major apolipoproteins made by the small intestine are apo A-I (13), apo A-II (21), apo A-IV (15,57), A-V (16), and apo B (13,23). Using [‘4C]oleate, [3H]leucine, and [i4C]glucosamine, Kessler et al. (28) found that the lipid, protein, and sugar of the intracellular CM precursor (pre-CM) are synthesized in the smooth ER, the rough ER, and the Golgi apparatus, respectively. It is important to note that these three organelles form the endomembrane system (33) and that, therefore, the formation of the various pre-CM components does not occur exclusively in any one organelle. For example, glycosylation of the newly synthesized protein involves both the ER and the Golgi apparatus (42). Christensen et al. (12) have reported that in fasting jejunal biopsies apolipoprotein B (apo B) label was found predominantly at the rough ER and within Golgi cistemae of the absorptive cells at the villus tip. During fat feeding, apo B label was found adjacent to both VLDL and CM within the apical smooth ER. The apo B label at the rough ER became less dense. Apo B label was also found at the rough ER and smooth ER junction. They concluded that apo B was synthesized in the rough ER, transferred to the smooth ER, and then added onto the lipoprotein particles. Both the Golgi vesicles and the cistemae had apo B label. This is the first demonstration of apo B being present not only on the surface of CM and VLDL, but also on the Golgi vesicle membrane. In the liver, it has been demonstrated that a considerable proportion of newly synthesized apo B is not associated with the lipoprotein, but rather with the membrane frac-
TABLE 1 CLASS DISTRIBUTION
OF PHOSPHOLIPIDS
Distribution, Prechylomicrons
Class
Phosphatidylcholine Phosphatidylethanolamine Lysophosphatidylcholine Sphingomyelin Phosphatidic acid Phosphatidylinositol
50.30 12.10 10.80 5.80 10.5 6.8
k t 2 + + ?
3.40$ 1.50? 2.22 1.24 2.26 0.82*
% Chylomicrons
80.20 2 0.41 4.40 + 0.65 4.50 2 0.55 6.60 5 0.48 4.20 2 0.29
Values are means k SE; n = 11 for prechylomicrons and 6 for chylomicrons. *p
0361-9230/91 $3.00 + .OO
0 Peqaraon Press plc, 1991. Printed in the U.S.A
The Absorption and Transport of Lipids by the Small Intestine PATRICK
TSO” AND KAZUMA
FUJIMOTO
Department of Physiology, Louisiana State University Medical Center, Shreveport, LA 71130
TSO, P. AND K. FUJIMOTO. The absorption and transport of lipids by the small infestine. BRAIN RES BULL 27(3/4) 477482, 1991. -Dietary lipid provides as much as 40% of the caloric intake in the Western diet. Triacylgiycerol is the main dietary fat. The human small intestine is also presented daily with II-12 g of phosphol~pid, predominantly phosphatidyicholine. The predominant sterol in the Western diet is cholesterol, which is derived from animal fat. Plant sterols account for up to 20-25% of total dietary sterol. This paper reviews our current unde~t~ding of the process and the factors that regulate the absorption and
transport of different dietary lipids by the human small intestine. Intestinal lipid absorption
Intestinal lipid metabolism
hydrolyzed to form predomin~tly 2-monoglyceride (MG) and fatty acid (FA) (6,ll). Experiments in vitro have demonstrated that the lipolytic action of lipase on a lipid emulsion containing TG and bile salts occurs slowly, resulting from the inhibition caused by bile salts at concentrations above critical micellar concentration (8). However, inhibition can be overcome by another protein in pancreatic juice called colipase (8). In the newborn, the pancreatic lipase system is not fully developed, and gastric lipase plays an important role in the digestion of milk fat. Readers interested in the subject of gastric lipase should refer to the review by Hamosh (22). Luminal PC is digested in the presence of pancreatic phospholipase A2 to form lysophosphatidylcholine (LPC) and fatty acid (FA) (34,43). Cholesterol can only be absorbed by the small intestine in the free form. Thus, dietary cholesteryl ester has to be hydrolyzed by cholesterol esterase (10) to form free cholesterol prior to absorption by the enterocytes.
NUMEROUS reviews have been written on the digestion and absorption of lipid by the small intestine (50,5 1). In this review, we will summarize our current understanding of how dietary lipid is digested and taken up by the epithelial cells (enterocytes) of the small intestine and of the factors regulating the intestinal formation and release of chylomicrons (CM) and very low-density lipoproteins (VLDL). DIETARY LIPIDS
As much as 40% of the daily caloric intake in the Western diet is in the form of lipids. Triacylglycerol (TG) is the major form of dietary fat in human beings and each glycerol backbone is esterified with three fatty acids (FA), mostly long-chain FA. common long-chain FA are palmitate (C 16:0), stearate (18:0), oleate (C l&l, w9), and linoleate (C 18:2, ~6). Because of the beneficial health effects associated with eating fish, there has been an increased consumption of fish or fish oil products. These benefits are related to the two major omega-3 FA present, eicosapentaenoate (C 205, ~3) and docosahexaenoate (C 22:6, ~3). In human milk formulas, 40-50% of the total calories are present as fat (22). The human small intestine is also presented daily with both dietary and endogenous phosp~olipids and sterols. Of the luminal phospholipids, phosphatidylcholine (PC) is by far the most important. Luminal PC can be derived from both the diet and from bile, but the biliary contribution (11-12 grams per day) (7,5.5) is significantly more than the dietary (l-2 grams per day) (7&S). The predominant sterol in the Western diet is cholesterol. However, plant sterols account for 20-25% of the total dietary sterol (51).
UPTAKE OF LIPID DIGESTION PRODUCTS BY THE ENTEROCYTE
Until very recently, it was generally believed that FA and MG are absorbed by the enterocytes through simple diffusion (50). However, the FA and MG have to overcome the diffusion barrier afforded by the “unstirred water layer” (59). This is achieved by the micellar solubilization of MG and FA by bile salts. Through micellar solubilization, the concentration of FA and MG next to the enterocyte membrane increases markedly, thus facili~ting the entry of these lipids into the enterocytes. MG and FA enter the enterocytes as monomers (50). Recent studies by Stremmel have indicated that there is a FA-binding protein associated with the brush-border membrane, and that this protein seems to play a role in the uptake of FA by enterocytes (47). While the data from Stremmel are certainly convincing, the
DIGESTION OF DIETARY LIPIDS
The bulk of TG digestion occurs in the duodenum of the small intestine. Through the action of pancreatic lipase, TG is -Kequests Ior reprints Should be 71130.
addressedto Dr. Patrick Tso, Department of Physiology,
477
L.S.U.
Med. Ctr., 1501 Kings Highway, Shreveport, LA
478
TSO AND FUJIMOTO
MONOACYLGLYCEROL
PATHWAY
1
0-Z-R
2 0 O-C-R
3 t 1
OH
2
OH
3t
-R._*
2
Phosphahdate Phosphohydrolase
opo,
3
Q
1 GLYCEROL
- 3 - PHOSPHATE
PATHWAY
2
c
.jt FIG.
I. Pathways of triacylglycerol biosynthesis
O-C-R 0 O-C-R
OPO-x
in the rat and hamster intestinal mucosa [adapted from (3O)l.
issue of whether FA is taken up by passive diffusion or by a carrier-mediated process warrants further investigation. Bergstedt et al. (5) have recently demonstrated that stearate seems to be taken up by the small intestine more slowly than oleate. It would be important to compare, both in vitro and in vivo, the uptake of long-chain FA by the small intestine. The uptake of LPC is believed to be passive. However, Stremmel has demonstrated that the brush-border membrane FA-binding protein also has the capacity to bind and transport LPC, thus raising the possibility that LPC transport may also be carriermediated. Uptake of cholesterol by the enterocytes is specific since B-sitosterol (a plant sterol), a molecule that bears considerable resemblance to cholesterol, is poorly absorbed. This specificity requires energy, as the deprivation of blood supply results in free permeability of different sterols (49). INTRACELLULAR METABOLISM OF ABSORBED LIPID DIGESTION PRODUCTS
As yet we do not know how the various absorbed lipids migrate from the site of absorption to the endoplasmic reticulum (ER) where biosynthesis of complex lipids takes place. A fatty acid binding protein present in the small intestine has been isolated and characterized by Ockner and Manning (35) which may play an important role in the intracellular transport of the absorbed FA. Nonetheless, we are still left with the question of how the other absorbed lipids, e.g., monoacylglycerol, get to the ER. Two sterol carrier proteins have been isolated and characterized (41,46), SCP-1 (47,000 mol.wt.) and SCP-2 (13,500 mol.wt.). SCP-1 is important in the microsomal conversion of squalene to lanosterol (46) and SCP-2 participates in the microsomal conversion of lanosterol to cholesterol (41). Although it has been suggested by some investigators that SCP-2 is also
the fatty acid binding protein, recent evidence by Scallen and co-workers (41) strongly indicates that these two are distinct proteins. Studies by Kharroubi et al. (29) have indicated that the SCP-2 isolated from intestinal epithelial cells is identical to the SCP-2 isolated from liver cytosol. As it does in other tissues, SCP-2 presumably plays an important role in the esterification of cholesterol to form ester and also in intracellular transport. 2-MG and FA are reconstituted to form TG mainly via the monoacylglycerol pathway. As shown in Fig. 1, 2-MG is reacylated into TG by the consecutive action of monoacylglycerol acyl transferase and diacylglycerol acyltransferase (27,30). The enzymes involved in this monoacylglycerol pathway are present in a complex called “triglyceride synthetase” (27). A number of studies have demonstrated that the enzymes involved in the MG pathway are located on the cytoplasmic surface of the ER (2). This finding has an important bearing on our understanding of the intracellular packaging of lipoproteins. The data would seem to indicate that TG is formed at the cytoplasmic surface of the ER and that somehow this TG gains entry into the cistemae of the ER. Based on the fact that TG has a low solubility in phospholipid bilayers (3 mol%), Small (45) postulated that TG molecules saturate the membrane rapidly. Once the solubility of TG is exceeded, Small suggests that TG splits the bilayer and forms a small lens that, as it grows, it bulges into either the cytoplasmic side or the cistemal side of the ER. He then suggests that this protrusion pinches off the membrane and forms either lipid droplets in the cytoplasm or precursors of lipoproteins in the cistemae of the ER. Small’s hypothesis has not been demonstrated experimentally. The other pathway present for the formation of TG in the intestinal mucosa is called the cr-glycerophosphate pathway (27,30). As shown in Fig. 1, this pathway involves the stepwise acyla-
INTESTINAL
479
LIPID ABSORPTION
tion of glycerol-3-phosphate to form phosphatidic acid. In the presence of phosphatidate phosphohydrolase, phosphatidic acid is hydrolyzed to form diacylglycerol (DG), which is then converted to TG. The relative importance of the MG pathway and the a-glycerophosphate pathway depends on the supply of 2-MG and FA. During normal lipid absorption, the 2-MG pathway is by far more important because of the extremely efficient conversion of 2-MG and FA to form TG and also because 2-MG inhibits the a-glycerophosphate pathway (27,30). However, when the supply of 2-MG is lacking or insufficient, the a-glycerophosphate pathway becomes the major pathway for the formation of TG. Some of the absorbed LPC is reacylated to form PC (34,43) and remainder is hydrolyzed to form glycero-3-phosphorylcholine (7,55). The liberated FA can be used for TG synthesis, while the glycerol-3-phyosphorylcholine can be readily transported via the portal blood for use in the liver (55). Cholesterol is transported almost exclusively by the lymphatic system, mainly as esterified cholesterol (CE). The rate of esterification of cholesterol may regulate the rate of lymphatic transport of cholesterol. Two enzymes have been proposed to be involved in the esterification, cholesterol esterase (4, 18, 56) and acyl-CoA cholesterol acyltransferase (ACAT) (4,25). Using immunocytochemistry, Gallo et al. (19) have demonstrated that intracellular cholesterol esterase is derived from pancreatic cholesterol esterase (19). A later study by Field (17) confirmed the presence of a cholesterol esterase in the enterocyte. It remains unclear how pancreatic cholesterol esterase is taken up by the enterocyte. There is a lack of general agreement on the relative importance of the two enzymes in the esterification of cholesterol by the enterocytes (4, 18, 56). Furthermore, the relative importance of the two enzymes in the esterification of cholesterol may depend on the exogenous cholesterol load (4). INTRACELLULAR
ASSEMBLY
OF LIPOPROTEINS
As we discussed earlier, the lipid droplet enters the cistemae of the ER. Through a mechanism as yet not well understood, the lipid droplet becomes associated with phospholipids and apolipoproteins. The major apolipoproteins made by the small intestine are apo A-I (13), apo A-II (21), apo A-IV (15,57), A-V (16), and apo B (13,23). Using [‘4C]oleate, [3H]leucine, and [i4C]glucosamine, Kessler et al. (28) found that the lipid, protein, and sugar of the intracellular CM precursor (pre-CM) are synthesized in the smooth ER, the rough ER, and the Golgi apparatus, respectively. It is important to note that these three organelles form the endomembrane system (33) and that, therefore, the formation of the various pre-CM components does not occur exclusively in any one organelle. For example, glycosylation of the newly synthesized protein involves both the ER and the Golgi apparatus (42). Christensen et al. (12) have reported that in fasting jejunal biopsies apolipoprotein B (apo B) label was found predominantly at the rough ER and within Golgi cistemae of the absorptive cells at the villus tip. During fat feeding, apo B label was found adjacent to both VLDL and CM within the apical smooth ER. The apo B label at the rough ER became less dense. Apo B label was also found at the rough ER and smooth ER junction. They concluded that apo B was synthesized in the rough ER, transferred to the smooth ER, and then added onto the lipoprotein particles. Both the Golgi vesicles and the cistemae had apo B label. This is the first demonstration of apo B being present not only on the surface of CM and VLDL, but also on the Golgi vesicle membrane. In the liver, it has been demonstrated that a considerable proportion of newly synthesized apo B is not associated with the lipoprotein, but rather with the membrane frac-
TABLE 1 CLASS DISTRIBUTION
OF PHOSPHOLIPIDS
Distribution, Prechylomicrons
Class
Phosphatidylcholine Phosphatidylethanolamine Lysophosphatidylcholine Sphingomyelin Phosphatidic acid Phosphatidylinositol
50.30 12.10 10.80 5.80 10.5 6.8
k t 2 + + ?
3.40$ 1.50? 2.22 1.24 2.26 0.82*
% Chylomicrons
80.20 2 0.41 4.40 + 0.65 4.50 2 0.55 6.60 5 0.48 4.20 2 0.29
Values are means k SE; n = 11 for prechylomicrons and 6 for chylomicrons. *p
