Hydrolysis of long-chain, n-3 fatty acid enriched chylomicrons by cardiac lipoprotein lipase

The hydrolysis of chylomicrons enriched in long-chain n-3 fatty acids by cardiac lipoprotein lipase was studied. In 60 min, 24.8% of the triacylglycerol fatty acids were released as free fatty acids. The fatty acids were hydrolyzed at different rates. DHA (docosahexaenoic acid, 22:6n-3) and EPA (eicosapentaenoic acid, 20:5n-3) were released at rates significantly less than average. Stearic acid (18:0), 20:1n-9, and alpha-linolenic acid (18:3n-3) were released significantly faster than average. There was no relationship between the rate of release of a fatty acid and the number of carbons or the number of double bonds. Lipoprotein lipase selectively hydrolyzes the fatty acids of chylomicron triacylglycerols. This selectively will result in remnants that are relatively depleted in 18:0, 20:1, and 18:3 and relatively enriched in 20:5 and 22:6.     

The effects of dietary n-3 polyunsaturated fatty acids delivered in chylomicron remnants on the transcription of genes regulating synthesis and secretion of very-low-density lipoprotein by the liver: modulation by cellular oxidative state

The influence of chylomicron remnants enriched in n-3 or n-6 polyunsaturated fatty acids (PUFA) (derived from fish or corn oil, respectively) on the expression of mRNA for four genes involved in the regulation of the synthesis, assembly, and secretion of very-low-density lipoprotein (VLDL) in the liver was investigated in normal rat hepatocytes and after manipulation of the cellular oxidative state by incubation with N-acetyl cysteine (NAC) or CuSO(4). The four genes investigated were those encoding apolipoprotein B (apoB), the microsomal triacylglycerol transfer protein (MTP), and the enzymes acyl coenzyme A:diacylglycerol acyltransferase (DGAT) and acyl coenzyme A:cholesterol acyltransferase 2 (ACAT2), which play a role in the regulation of triacylglycerol and cholesteryl ester synthesis, respectively. mRNA levels for apoB, MTP, and DGAT were unaffected by either fish or corn oil chylomicron remnants, but the amount of ACAT2 mRNA was significantly reduced after incubation of the hepatocytes with fish oil remnants as compared with corn oil remnants or without remnants. These findings indicate that the delivery of dietary n-3 PUFA to hepatocytes in chylomicron remnants downregulates the expression of mRNA for ACAT2, and this may play a role in their inhibition of VLDL secretion. However, when the cells were shifted into a pro-oxidizing or pro-reducing state by pretreatment with CuSO(4) (1 mM) or NAC (5 mM) for 24 hr, levels of mRNA for MTP were increased by about 2- or 4-fold, respectively, by fish oil remnants, whereas corn oil remnants had no significant effect. Fish oil remnants also caused a smaller increase in apoB mRNA in comparison with corn oil remnants in NAC-treated cells (+38%). These changes would be expected to lead to increased VLDL secretion rather than the decrease associated with dietary n-3 PUFA in normal conditions. These findings suggest that relatively minor changes in cellular redox levels can have a major influence on important liver functions such as VLDL synthesis and secretion.     

Comparison of the metabolic effects of chylomicrons and their remnants on isolated hepatocytes

A comparison was made between the effects of chylomicrons and chylomicron remnants on metabolic processes of isolated hepatocytes. Since isolated triacylglycerol-rich lipoproteins are contaminated with nonesterified fatty acids, control incubations were conducted with an amount of fatty acid equivalent to the contaminating fatty acids present in the chylomicrons and the remnant preparations, respectively. Chylomicron remnants, produced in vitro by incubation of chylomicrons in postheparin rat plasma, caused marked inhibition of glycolysis, fatty acid synthesis, and cholesterol synthesis, along with marked stimulation of ketogenesis. These effects were traced to the release of nonesterified fatty acids from these remnant particles as a consequence of contamination with lipoprotein lipase, picked up by the particles during the incubation with rat plasma. Fatty acids inhibit glycolysis, cholesterol, and fatty acid synthesis, but enhance ketone body formation by isolated hepatocytes. Chylomicrons and remnants prepared in vivo by the injection of chylomicrons into functionally hepatectomized rats were not contaminated with lipoprotein lipase and did not inhibit glycolysis and cholesterol synthesis nor increase ketone body formation. These lipoprotein particles did, however, cause significant inhibition of fatty acid synthesis, with the chylomicrons being more effective on a protein basis than the remnants produced in vivo. The mechanism responsible for the inhibition of fatty acid synthesis by chylomicrons and remnants prepared in vivo remains to be resolved.     

The effect of triacyl-sn-glycerol structure on the metabolism of chylomicrons and triacylglycerol-rich emulsions in the rat

A systematic study was undertaken to observe the effects of dietary (dioleoyl) triacyl-sn-glycerol structure on chylomicron composition and metabolism. First studied was a series of 1,2-dioleoyl-3-(saturated)acyl-sn-glycerols, where the fatty acid esterified at the 3-position was varied from 14 to 24 carbons. Next a series of 1,3-dioleoyl-2-acyl glycerols was studied, with various fatty acids esterified at the glycerol 2-position. These stereospecific triacyl-sn-glycerols were fed to donor rats and lymph chylomicrons were isolated, analyzed, and reinjected into recipient rats to study their disappearance from plasma and delivery to tissues. As shown by their compositions, chylomicrons obtained after feeding triacylglycerols containing all sn-3 fatty acid of chain length greater than 20 carbons were under-represented, possibly due to poorer digestion by lipases, or poorer absorption by the intestine. The 18-carbon saturated chain fatty acid (stearic acid) was equally well represented in chylomicrons whether in the 2- or 3-position of the fed triacylglycerol. The presence of increased amounts of long-chain saturated fatty acids in donor chylomicron triacylglycerols affected the metabolism of chylomicrons injected into the bloodstream of recipient rats. In particular the rate of removal of labeled cholesteryl esters, tracing removal of the partially degraded chylomicron remnants was slowed by the saturated chains, with palmitic acid and the 20-carbon fatty acid, arachidic acid, showing the most severe effects. There were clear differences in the removal from plasma of injected lymph chylomicrons derived from fed triacylglycerols containing stearic acid in either the 2- or 3-position, with evidence for remnants from the symmetrical triacylglycerols being less rapidly removed from the circulating blood. This effect was investigated further by injected model emulsions of chylomicrons, where the 2-position was substituted with saturated or transunsaturated acyl chains. Quantitation of removal from the blood stream of these model lipoproteins confirmed that a saturated or transunsaturated long chain fatty acid at the 2-position of the emulsion triacylglycerols slowed remnant removal from the blood. In some cases, with both lymph chylomicron and with emulsions, the lipolytic step mediated by lipoprotein lipase was also slowed.     

The biosynthesis of docosahexaenoic acid [22:6(n-3)] from linolenic acid in primary hepatocytes isolated from wild northern pike

Primary hepatocytes from wild northern pike Esox lucius were incubated with radiolabelled linolenic acid ([l-¹⁴C]-18:3(n-3)) to assess their ability to synthesize docosahexaenoic acid [22:6(n-3)]. The distribution of radioactivity in lipid classes and hepatocyte polyunsaturated fatty acids (PUFA) was measured over the time-course of 24h. The majority of radioactivity from [l-¹⁴C]-18:3(n-3) was recovered in hepatocyte triacylglycerols (TAG) and phosphatidylcholine (PC). The levels of radioactivity in TAG and in most of phospholipids, including PC, increased significantly over the incubation period. Radioactivity from [1-¹⁴C]-18:3(n-3) was recovered in several hepatocyte PUFA, including 22:6(n-3), and the Δ6 and Δ5-desaturation products 18:4(n-3) and 20:5(n-3). The presence of radioactivity in C₂₄ (n-3) PUFA may be evidence that the biosynthesis of 22:6(n-3) in pike proceeds via a pathway independent of Δ4-desaturation. Analysis by radio gas chromatography revealed that radiolabelled 24:6(n-3) was present among the desaturation and elongation products of [l-¹⁴C]-18:3(n-3). The results establish that, under the in vitro conditions employed, pike hepatocytes are able to convert linolenic acid to 20:5(n-3) and 22:6(n-3).     

Chylomicron remnant induction of lipid accumulation in J774 macrophages is associated with up-regulation of triacylglycerol synthesis which is not dependent on oxidation of the particles

The influence of chylomicron remnants on lipid accumulation and synthesis and the activity and/or expression of mRNA for some of the key enzymes involved was investigated in the murine macrophage cell line J774. The effects of varying the polyunsaturated fatty acid (PUFA) composition and oxidation state of the remnants were also examined. Chylomicron remnants derived from corn oil (rich in n-6 PUFA) or fish oil (rich in n-3 PUFA) were prepared in vivo and oxidised by incubation with CuSO(4). The native and oxidised remnants caused a marked rise in intracellular triacylglycerol levels, but the rise induced by corn oil remnants (four- to sixfold) was greater than that observed with fish oil remnants (<2-fold). Triacylglycerol synthesis, as measured by the incorporation of [3H]oleate and [3H]glycerol into cellular triacylglycerol, was increased by all four remnant types tested, and corn oil remnants had a significantly greater effect than fish oil remnants. Oxidation of the remnants did not affect the results obtained. Although the incorporation of [3H]oleate into cholesteryl ester by the cells was not significantly changed by any of the four types of remnants tested, the activity and expression of mRNA for acyl Co-enzyme A: cholesterol acyltransferase (ACAT) was increased by corn oil, but not by fish or oxidised corn, remnants. Neutral cholesteryl ester hydrolase (nCEH) activity, however, was also raised by corn oil remnants. These studies indicate that chylomicron remnants induce the accumulation of triacylglycerol in J774 macrophages, and that increased synthesis of triacylglycerol plays a major role in this process. Furthermore, they demonstrate that these effects are enhanced when the remnants are enriched in n-6 PUFA as compared with n-3 PUFA, but not after oxidation of the particles, suggesting that the fatty acid composition of chylomicron remnants may be more important than their oxidation state in their ability to induce foam cell formation.     

Effects of exogenous apo E-3 and of cholesterol-enriched meals on the cellular metabolism of human chylomicrons and their remnants

The effects of exogenous apo E-3 and of cholesterol-enriched meals on the binding, cell association and proteolytic degradation of human chylomicrons and their remnants were determined in cultured human skin fibroblasts. Chylomicrons were prepared from plasma of normolipemic humans 4 h after a fat meal with normal or high cholesterol content. Remnants were obtained after incubation of chylomicrons with lipoprotein lipase in vitro. Cellular metabolism of chylomicrons was minimal, less than 10% that of LDL. Exogenous apo E-2 enhanced chylomicron metabolism by 3-4-fold. The cellular metabolism of remnants was 2.5-3.5-fold higher as compared to intact chylomicrons but their response to exogenous apo E-3 was considerably lower. The cellular metabolism of chylomicrons and chylomicron remnants obtained from subjects eating cholesterol-enriched fat meal was the highest either without or with added exogenous apo E-3. Yet, even in the preparation that exhibits the highest metabolic activity (apo E-3 enriched remnants from cholesterol-enriched meals) the absolute proteolytic degradation was about two-thirds that of LDL. We conclude that although LDL-receptors take up and degrade chylomicron remnants, the rate of catabolism of remnants by this route can not explain the rapid and complete remnant removal process as observed in vivo.     

Hepatic uptake of phospholipid-depleted chylomicrons in vivo. Comparison with the uptake of chylomicron remnants.

1. Rats pretreated with Triton WR-1339 to prevent the formation of remnants were injected with [3H]cholesterol-labelled remnants, intact chylomicrons or chylomicrons depleted of most of their surface phospholipids by treatment with phospholipase A2. Within 5 min about 80% of the injected label of remnants and phospholipid-depleted chylomicrons was incorporated into the livers compared with less than 10% of the injected radioactivity of intact chylomicrons. A similar rapid hepatic uptake of radioactivity occurred when rats not pretreated with Triton were injected with [3H]cholesterol-labelled phospholipid-depleted chylomicrons. This rapid hepatic uptake of phospholipid-depleted chylomicrons occurred apparently without any alteration in the apoprotein composition of the particles. 2. The participation of hepatocytes in the uptake of remnants and phospholipid-depleted chylomicrons was examined. Both types of particles were taken up by the hepatocytes. However, small chylomicrons (Sf less than 400) were taken up more efficiently than were large chylomicrons (Sf greater than 400), but neither was taken up as efficiently as the remnants. 3. The results of this study lend support to the hypothesis that phospholipid-depleted chylomicrons and chylomicron remnants are taken up by the liver by a similar mechanism, which depends on the loss of surface phospholipids.     

Plasma clearance and liver uptake of chylomicron remnants generated by hepatic lipase lipolysis: evidence for a lactoferrin-sensitive and apolipoprotein E-independent pathway

Chylomicrons labeled with [3H]cholesterol and [14C]triglyceride fatty acids were lipolyzed by hepatic lipase (HL) in vitro and then injected intravenously into normal mice fed low- or high-fat diets, and into apolipoprotein (apo) E-deficient mice. In normal mice fed the high-fat diet and injected with non-lipolyzed chylomicrons, the plasma clearance and hepatic uptake of the resulting [3H]cholesterol-labeled remnants was markedly inhibited. In contrast, chylomicrons lipolyzed by HL were taken up equally rapidly by the livers of mice fed the low- and high-fat diets. The removal of non-lipolyzed chylomicrons lacking apoE from the plasma of apoE-deficient mice was inhibited, but not the removal of chylomicrons lipolyzed by HL. Pre-injection of lactoferrin into normal mice inhibited the plasma clearance of both non-lipolyzed chylomicrons and chylomicrons lipolyzed by HL. The removal of HL from the surface of the lipolyzed particles by proteolytic digestion did not affect their rapid uptake, indicating that the hepatic recognition of the lipoproteins was not mediated by HL. These observations support previous findings that phospholipolysis of chylomicrons by hepatic lipase generates remnant particles that are rapidly cleared from circulation by the liver. They also support the concept that chylomicron remnants can be taken up by the liver by an apolipoprotein E-independent mechanism. We hypothesize that this mechanism is modulated by the remnant phospholipids and that it may involve their interaction with a phospholipid-binding receptor on the surface of hepatocytes such as the class B scavenger receptor BI.     

Fatty acid composition of platelet phospholipids and plasma lipids in obese Zucker rats

The purpose of this work was to see whether hyperlipaemia observed in genetically obese Zucker rats (fa/fa) was associated with differences in fatty-acid composition of plasma triacylglycerols, plasma phospholipids and of platelet phospholipids, in comparison with the control lean rats (Fa/-). Results showed that plasma triacylglycerols and phospholipids were increased in obese rats. In triacylglycerols, the amount of saturated and monounsaturated fatty acids was highly increased whereas the amount of the n-6 and n-3 polyunsaturated fatty acids was little modified. In plasma phospholipids, saturated and monounsaturated fatty acids were also increased, as were the n-3 fatty acids (except C 18:3 n-3); the n-6 fatty acids were little increased except C 20:3 n-6 which was markedly increased. These results concerning the amounts of fatty acids have their counterpart in their relative proportions of fatty acids. Data thus obtained suggest that conversion of linoleic acid (C 18:2 n-6) into arachidonic acid (C 20:4 n-6) was decreased in obese rats, particularly the delta 5 desaturation step. On the contrary, conversion of linolenic acid (C 18:3 n-3) into higher polyenes seemed increased. Thrombocytosis was not modified in the obese rat, but the volume of the platelets was increased. Platelet phospholipids exhibited the same modifications as plasma phospholipids but with different magnitude. Saturated and monounsaturated fatty acids were little augmented, n-3 fatty acids were more augmented (except C 18:3 n-3 acid which was unchanged); n-6 fatty acids were not modified except C 20:3 n-6 acid which was highly increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transport of n-3 fatty acids from the intestine to the retina in rats.

This study was undertaken to determine the mode of transport of the essential (n-3) fatty acids docosahexaenoic acid 22:6(n-3) and linolenic acid 18:3(n-3). Male weanling Sprague-Dawley rats received a mixture of corn oil and [14C]18:3(n-3) or [14C]22:6(n-3) by gavage. At periods of 1 to 4 days after the injection, four rats per time point were killed and samples of blood were taken via heart puncture and the livers and retinas were collected. Blood lipoproteins and plasma proteins were separated by ultracentrifugation and analyzed by HPLC. Lipids were extracted and saponified and the fatty acids were converted to phenacyl esters for separation of individual fatty acids. After 1 and 2 h, radioactivity from 18:3(n-3) and 22:6(n-3) was observed primarily in the chylomicron/very low density lipoprotein fraction. By 4 h, radioactivity in the lipoprotein fraction was greatly decreased, with a small amount of radioactivity associated with albumin in the soluble protein fraction. After 24 h, the total amount of radioactivity associated with lipoprotein was further reduced, with more than half of the remaining label occurring in association with albumin and another unidentified protein. In the liver, 22:6(n-3) was concentrated in triacylglycerols (40.7%) and phospholipids (51.1%), with a maximum specific activity at 4 h. In the rod outer segments (ROS), the specific activity of [14C]22:6(n-3) increased to a maximum at 24 h and maintained a high level even at 4 days. These data suggest that after injection, 18:3(n-3) and 22:6(n-3) are esterified to triglyceride and phospholipid by the intestinal absorptive cells and transported in chylomicrons to the liver. After conversion of 18:3(n-3) to 22:6(n-3) in the liver, the retina accumulates 22:6(n-3) which may be transported from the liver via albumin and another unidentified protein, and is retained by the rod outer segments.     

Modification of fatty acid composition of membrane phospholipid in hepatocyte monolayer with n-3, n-6 and n-9 fatty acids and its relationship to triacylglycerol production

The objective of these studies with rat hepatocytes in primary culture was to establish that: (a) membrane phospholipids would become enriched with the specific fatty acid supplemented to the media and (b) hepatocyte monolayer triacylglycerol synthetic rates were dependent on the type of fatty acid enrichment of the membrane phospholipids. Hepatocytes cultured in the absence of media lipid developed a phospholipid fatty acid composition which is indicative of an essential fatty acid deficiency. The extensive rise in 18:1(n - 9) content indicated that delta 9-desaturase was active. The fatty acid composition of phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol in the microsomal- and mitochondrial-enriched fractions was highly dependent upon the type of fatty acid supplemented to the medium. Incorporation of fatty acids into phospholipids was rapid, and a new steady-state in fatty acid composition was achieved within approx. 36 h. Changes in the fatty acid composition of these hepatocyte phospholipid subclasses resulting from media supplementation with 18:2/20:4(n-6) or 20:5(n-3) were similar, but not identical, to changes which occurred in vivo as a result of consuming diets rich in 18:2(n-6) or 20:5(n-3). Hepatocyte lipogenesis was highly dependent upon the type of fatty acid supplemented to the medium. Prior conditioning with 16:0 increased triacylglycerol synthesis and secretion. Secretion of triacylglycerol was reduced by polyenoic fatty acid enrichment with 20:5(n-3) greater than 20:4/18:2(n-6). The suppression of triacylglycerol synthesis by 20:5(n-3) was due to an increased (P less than 0.05) diacylglycerol specific activity, which indicates that 20:5(n-3) suppression of hepatic triacylglycerol production may be caused in part by the inhibition of diacylglycerol acyltransferase.     

Comparison of the metabolism of chylomicrons and chylomicron remnants by the perfused liver

1. The hepatic metabolism of chylomicrons and chylomicron remnants was compared after adding approximately equal numbers of each lipoprotein particle to the perfusate of isolated livers. 2. At least 40% of the added remnants were metabolized by the liver compared with less than 3% for chylomicrons. 3. There was significantly more net removal of labelled remnants than of chylomicrons by the liver. 4. A greater proportion of labelled cholesterol than of labelled triacylglycerol fatty acids was transferred to the liver from each lipoprotein. 5. Cholesteryl esters of remnants were hydrolysed to triacylglycerol fatty lipoprotein. 5. Cholesteryl esters of remnants were hydrolysed to triacylglycerol fatty acids of remnants were oxidized to CO2 more extensively than those of chylomicrons. 6. There was greater oxidation of remnant glycerolipic [(1(-14)C]oleate than of glycerolipid [1(-14)C]palmitate. 7. A large fraction of the fatty acids of remnants, but not of chylomicrons, was transferred to phospholipids, which were released by the liver in a lipoprotein of relative density less than 1.006. 8. Label from remnants, but not from chylomicrons, was found in lipoproteins of relative density greater than 1.006, which were not released during perfusion but could be flushed out from the liver at the end of perfusion.     

Change in fatty acid composition of serum lipids in obese females after short-term weight-reducing regimen with the addition of n-3 long chain polyunsaturated fatty acids in comparison to controls

Short-term weight-reducing regimens were shown to influence fatty acid composition of serum lipids unfavorably. Adding long chain n-3 polyunsaturated fatty acids (n-3 LC PUFA) to a low-calorie diet (LCD) could avoid these changes. The aim of this study was to examine the effect of a short-term in-patient weight-reducing regimen including LCD with yogurt enriched by low doses of n-3 PUFA (n-3 LCD). The enriched yogurt contained 790 mg of fish oil, predominantly eicosapentaenoic (20:5n-3; EPA) and docosahexaenoic (22:6n-3; DHA). Forty obese women were randomly assigned to the group consuming LCD and joghurt either with or without n-3 enrichment. Following the 3-week diet in the n-3 LCD group a significantly higher increase in the proportion of n-3 LC PUFA (sum of n-3 FA, EPA and DHA) in serum lipids was confirmed. In phospholipids (PL) a significant difference in the sum of n-6 fatty acids was found, a decrease in the n-3 LCD group and an increase in LCD group. Significantly higher increase in the PL palmitate (16:0) was shown in the LCD group. The results suggest that low doses of n-3 fatty acid enrichment can help to avoid unfavorable changes in fatty acid composition in serum lipids after a short-term weight-reducing regimen.     

The 1990 Borden Award Lecture. Dietary regulation of fatty acid and triglyceride metabolism.

The level of circulating triacylglycerols is determined by the balance between their delivery into the plasma and their removal from it. Plasma triacylglycerols are derived either from dietary fat as chylomicrons or from endogenous hepatic synthesis as very low density lipoproteins. Their removal occurs through the action of lipoprotein lipase after which the fatty acids are either stored in adipose tissue or oxidized, primarily in skeletal muscle and heart. The composition of the diet has been shown to influence many of these processes. Hepatic fatty acid synthesis and triacylglycerol secretion are affected by the quantity and composition of dietary fat, carbohydrate, and protein. Polyunsaturated but not saturated fats reduce hepatic fatty acid synthesis by decreasing the amount of the lipogenic enzymes needed for de novo fatty acid synthesis. Dietary fish oils are particularly effective at reducing both fatty acid synthesis and triacylglycerol secretion and as a result are hypotriacylglycerolemic, particularly in hypertriacylglycerolemic individuals. In addition, dietary fish oils can increase the oxidation of fatty acids and lead to increased activity of lipoprotein lipase in skeletal muscle and heart. It appears that the hypotriacylglycerolemic effect of dietary fish oils is mediated by effects on both synthesis and removal of circulating triacylglycerols.     

The lipid composition of two species of serrasalmid fish in relation to dietary polyunsaturated fatty acids

The lipid composition of two species of Serrasalmid fish with different natural feeding habits were compared in relation to the polyunsaturated fatty acids (PUFA) supplied in their diets. Mylossoma aureum , a herbivorous piranha, was maintained on oatmeal flakes in which : 2(n-6) and : 3(n-3) were the only PUFA and accounted for 40–8 and 1.2%, respectively of dietary fatty acids. Serrasalmus nattereri , the carnivorous red piranha, was fed mosquito larvae containing .0-33.4% of their total fatty acids as : 2(n-6)+18 : 3(n-3) and 4.9-8.5% as 20 : 4(n-6)+20 : 5(n-3). The two species had similar lipid class compositions in liver, brain, viscera and carcass, except that lipids from M. aureum were generally richer in triacylglycerols. In both species, visceral and carcass lipid contained high levels of triacylglycerols whose principal PUFA was : 2(n-6). In M. aureum the major PUFA in liver total lipid and triacylglycerols was : 2(n-6) whilst the major PUFA in liver phospholipids were : 4(n-6) and : 5(n-6), with : 6(n-3) being a minor component. The level of : 6(n-3) in ethanolamine glycerophospholipids was significantly greater in brain than liver of M. aureum. Although absent from dietary lipid, : 6(n-3) was the major PUFA in phosphatidylcholine and ethanolamine glycerophospholipids from both the liver and brain of S, nattereri . In both species, the ratio of (n-6)/(n-3)PUFA was consistently lower in tissue lipids than in dietary lipids. The results are consistent with (i) the herbivorous M. aureum converting dietary C18 PUFA to their C20 and C22 homologues, (ii) the carnivorous S, nattereri forming : 6(n-3) from either 18:3(n-3) or 20: 5(n-3) and (iii) both species selectively desaturating and elongating (n-3) rather than (n-6) PUFA.     

Phospholipids as modulators of hepatic recognition of chylomicron remnants. Observations with emulsified lipoprotein lipids.

The lipids extracted from chylomicrons, chylomicron remnants generated in vivo and hepatic-lipase-treated chylomicrons were emulsified by sonication. These emulsified particles retained the capacity of the native lipoproteins to be differentiated by the liver in vivo, i.e. only the particles derived from remnant and hepatic-lipase-treated chylomicron lipids were efficiently taken up by the liver. To investigate the role of phospholipids in this differentiation process, the phospholipids of all three lipoprotein preparations were separated from the remaining lipids by silicic acid chromatography. The phospholipid-free lipid fraction of chylomicrons was then emulsified with the phospholipids derived from each of the three lipoprotein preparations. Only the particles emulsified with phospholipids derived from remnants and hepatic-lipase-treated chylomicrons were efficiently taken up by the liver in vivo. These results support the proposition that phospholipids modulate the hepatic differentiation between chylomicrons and remnants in vivo.