Diagnosis, Outcome, and Management of Chylous Ascites Following Pediatric Liver Transplantation.

Data on postoperative chylous ascites (CA) after pediatric liver transplantation (LT) are scarce. This retrospective study was conducted to identify the incidence, risk factors, management, and outcomes of postoperative CA in a large single-center pediatric LT cohort (2000-2016). The study cohort comprised 317 LTs (153 living donors and 164 deceased donors) in 310 recipients with a median age of 2.7 years. The incidence of CA was 5.4% (n = 17), diagnosed after a median time of 10 days after LT. Compared with chylomicron detection in peritoneal fluid (the gold standard), a triglyceride cutoff value of 187 mg/dL in peritoneal fluid showed insufficient sensitivity (31%) for CA diagnosis. In univariate logistic regression analyses, ascites before LT, younger age, and lower weight, height, and height-for-age z score at LT were associated with CA. Symptomatic management of CA included peritoneal drain (100%) and diuretics (76%). Therapeutic interventions included very low-fat or medium-chain triglyceride-rich diets (94%) and intravenous octreotide (6%), leading to CA resolution in all patients. CA was associated with prolonged hospital length of stay (LOS; 40 days in the CA group versus 24 days in the non-CA group; P = 0.001) but not with reduced patient or graft survival rates after a median follow-up time of 14 years. In conclusion, CA in the pediatric LT recipient is a relatively uncommon complication associated with increased hospital LOS and morbidity. Measurement of chylomicrons is recommended in patients with ascites that is more severe or persistent than expected. Dietary interventions are effective in most patients.

Characterization of chylomicron in preterm infants.

BACKGROUND: The aim of this study was to investigate cholesterol and triglyceride levels in the chylomicron fraction of preterm infants at birth and during the early postnatal period. METHODS: The subjects consisted of 133 infants (81 boys and 52 girls): 74 were term infants born at 37-41 weeks of gestation and 59 were preterm infants born at 29-36 weeks of gestation. Cholesterol and triglyceride in the chylomicron fraction were measured using high-performance liquid chromatography. RESULTS: Compared with term infants, preterm infants had higher cholesterol and lower triglyceride in the chylomicron fraction, both in cord blood and at 1 month after birth. Thus, the chylomicron triglyceride/cholesterol ratio was significantly lower in preterm infants than in term infants in cord blood and at 1 month of age. On single regression analysis the chylomicron triglyceride/cholesterol ratio correlated positively with gestational age at birth (r = 0.331, P = 0.0003) and at 1 month (r = 0.221, P = 0.0119). CONCLUSIONS: Preterm infants have a less-lipidated chylomicron composition at birth and at 1 month of age. Some prenatal factors may persist to influence chylomicron lipidation during the early postnatal period.

Analysis of cholesterol levels in lipoprotein(a) with anion-exchange chromatography.

We previously established an analysis method for determining the cholesterol levels of five major lipoprotein classes [HDL, LDL, intermediate density lipoprotein (IDL), VLDL, and chylomicrons] in serum by an anion-exchange (AEX)-HPLC method, but lipoprotein(a) [Lp(a)], a well-known risk factor for atherosclerotic diseases, was not determinable. Therefore, we established new AEX-HPLC separation conditions for analyzing the cholesterol levels of six lipoprotein classes, including Lp(a). Serum lipoproteins were separated by HPLC with a diethylaminoethyl-ligand nonporous polymer-based column by elution with a stepwise gradient of the sodium perchlorate concentration. In this improved method, HDL, LDL, IDL, VLDL, chylomicrons, and Lp(a) were each eluted from the column. The cholesterol levels of the eluted lipoproteins were measured enzymatically by a postcolumn reaction. The within-day assay and between-day assay coefficients of variation for the lipoprotein cholesterol levels were in the ranges of 0.29-11.86% and 0.57-11.99%, respectively. The Lp(a) cholesterol levels determined by AEX-HPLC were significantly correlated with the amounts of Lp(a) protein measured by an immunoturbidimetry method available commercially (r = 0.9503, P < 0.0001). Taken together, this AEX-HPLC method may be effectively applied to the analysis of serum lipoproteins with high levels of Lp(a).

Sites of lipoprotein lipase activity in adipose tissue perfused with chylomicrons. Electron microscope cytochemical study.

Lipoprotein lipase activity was studied in rat parametrial adipose tissue perfused with chylomicrons and in gelatin blocks containing postheparin plasma and chylomicrons. The tissues and blocks were fixed in glutaraldehyde and incubated in 0.035 M CaCl(2)-0.1 M Tris medium (pH 8.3) at 38 degrees C. The doubly labeled chylomicron triglycerides (glycerol-(3)H and palmitate-(14)C) in the tissues and blocks were hydrolyzed during incubation to free fatty acids (FFA) and the FFA remained in the specimens; hydrolysis was inhibited by 0.004 M diethyl paranitrophenyl phosphate (E-600). Incubated blocks and tissue were treated with 0.05 M Pb(NO(3))(2), postfixed in OsO(4), dehydrated with acetone, embedded in Epon, and examined by electron microscopy. The incubated blocks contained electronlucent areas and granular and laminar precipitates at sites of hydrolysis. Similar precipitates were found in incubated tissue, within vacuoles and microvesicles of capillary endothelium, and in the subendothelial space (between the endothelium and pericytes), but not in the capillary lumen or in or near fat cells. The cytochemical reaction was greatly reduced, in blocks and tissues incubated with E-600. It is concluded that plasma glycerides are hydrolyzed by lipoprotein lipase in capillary endothelial cells and in the subendothelial space of adipose tissue and that glycerides across the endothelial cells within a membrane-bounded system.

Vitamin A concentrations in piglet extrahepatic tissues respond differently ten days after vitamin A treatment.

Periodic supplementation to infants and young children is encouraged in developing countries by the WHO. We investigated vitamin A (VA) in extrahepatic tissues of piglets after supplementation with retinyl acetate to determine long-term storage. 3, 4-Didehydroretinyl acetate (DRA) as a tracer was used to evaluate uptake from chylomicra in 4 h. Sows were fed a VA-depleted diet throughout pregnancy and lactation. Male castrated piglets (n = 28, 11.6 +/- 0.5 d) from these sows were weaned onto a VA-free diet for 1 wk, assigned to 4 groups, and dosed orally with 0, 26.2, 52.4, or 105 micromol VA. After 10 d, 5.3 micromol DRA was administered to determine short-term uptake of 3, 4-didehydroretinol (DR). Four hours later, piglets were killed; adrenal glands, kidney, lung, and spleen were collected and analyzed for retinol and DR. Retinol concentrations of kidney and adrenal gland were higher than control, but treated groups did not differ. Retinol concentration was highest in kidney (1.70-2.52 nmol/g), followed by adrenal gland (0.30-0.48 nmol/g), lung (0.15-0.21 nmol/g), and spleen (0.11-0.15 nmol/g). Total retinol in kidney and spleen was different among the groups (P < 0.05). Unesterified retinol was the major VA form; the percent retinol of total VA was lowest in adrenal glands. DR did not differ among the groups. In 4 h, the minimum estimated chylomicron contribution to tissue DR was 63-280% higher than the maximum DR exposure from retinol-binding protein. Constant dietary intake may be important in maintaining VA concentrations in extrahepatic tissues.

Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Apolipoprotein (apo) E and the two B apolipoproteins, apoB48 and apoB100, are important proteins in human lipoprotein metabolism. Commonly occurring polymorphisms in the genes for apoE and apoB result in amino acid substitutions that produce readily detectable phenotypic differences in these proteins. We studied changes in apoE and apoB phenotypes before and after liver transplantation to gain new insights into apolipoprotein physiology. In all 29 patients that we studied, the postoperative serum apoE phenotype of the recipient, as assessed by isoelectric focusing, converted virtually completely to that of the donor, providing evidence that greater than 90% of the apoE in the plasma is synthesized by the liver. In contrast, the cerebrospinal fluid apoE phenotype did not change to the donor's phenotype after liver transplantation, indicating that most of the apoE in CSF cannot be derived from the plasma pool and therefore must be synthesized locally. The apoB100 phenotype (assessed with immunoassays using monoclonal antibody MB19, an antibody that detects a two-allele polymorphism in apoB) invariably converted to the phenotype of the donor. In four normolipidemic patients, we determined the MB19 phenotype of both the apoB100 and apoB48 in the "chylomicron fraction" isolated from plasma 3 h after a fat-rich meal. Interestingly, the apoB100 in the chylomicron fraction invariably had the phenotype of the donor, indicating that the vast majority of the large, triglyceride-rich apoB100-containing lipoproteins that appear in the plasma after a fat-rich meal are actually VLDL of hepatic origin. The MB19 phenotype of the apoB48 in the plasma chylomicron fraction did not change after liver transplantation, indicating that almost all of the apoB48 in plasma chylomicrons is derived from the intestine. These results were consistent with our immunocytochemical studies on intestinal biopsy specimens of organ donors; using apoB-specific monoclonal antibodies, we found evidence for apoB48, but not apoB100, in donor intestinal biopsy specimens.

Abnormal lipid composition of chylomicrons in broad-beta disease (type 3hyperlipoproteinemia).

Chylomicron (primary particles) were detected by polyvinylpyrollidone (PVP) flocculation in plasma collected after an overnight fast from eight hyperlipemic subjects with broad-beta disease (type III hyperlipoproteinemia). The composition of these chylomicrons was abnormal: relatively poor in triglyceride and rich in cholesterol, giving rise to a triglyceride/cholesterol ratio of < 3.0 in all cases, uniformly below the ratio in chylomicrons from eight fasting subjects with mixed lipemia. By contrast, at the peak of alimentary lipemia following an oral fat load (2 g/kg), chylomicrons from broad-beta subjects had normal, triglyceride-rich composition (triglyceride/cholesterol = 14.0) and resembled chylomicrons from subjects with mixed lipemia, endogenous lipemia, and familial hypercholesterolemia after similar fat loads. As the alimentary lipemia cleared, chylomicrons remaining in broad-beta subjects 14-24 hr after the fat load were again rich in cholesterol. However, a similar degree of cholesterol enrichment was observed in chylomicrons from the subjects with familial hypercholesterolemia, while only a minor increase in cholesterol was recorded in chylomicrons from subjects with mixed or endogenous lipemia. Parallel studies of changes in chylomicron composition during in vitro incubation of whole plasma and of S(f) > 400 with S(f) < 400 lipoproteins from subjects with the different forms of hyperlipoproteinemia revealed equal cholesterol enrichment of chylomicrons from a subject with mixed lipemia and from a subject with broad-beta disease in media of equivalent cholesterol content. These experiments suggested neither excessive avidity of chylomicrons for cholesterol uptake nor excessive influence of S(f) < 400 lipoproteins upon chylomicron composition in broad-beta disease.Thus, results in this study suggest that the cholesterol-rich chylomicrons observed in subjects with broad-beta disease after an overnight fast may originate in the intestine as particles of normal composition (chiefly dietary triglyceride) but assume a composition which is relatively rich in cholesterol through processes of lipolysis and cholesterol transfer among circulating lipoproteins which may not be unique to broad-beta disease.

Synthesis and transport of lipoprotein particles by intestinal absorptive cells in man.

The site of synthesis and some new details of lipoprotein particle transport have been demonstrated within the jejunal mucosa of man. In normal fasting volunteers, lipoprotein particles (88%, 150-650 A diameter) were visualized within the smooth endoplasmic reticulum and Golgi cisternae of absorptive cells covering the tips of jejunal villi. Electron microscopic observations suggested that these particles exited through the sides and bases of absorptive cells by reverse pinocytosis and then passed through the extracellular matrix of the lamina propria to enter lacteal lumina. When these lipid particles were isolated from fasting intestinal biopsies by preparative ultracentrifugation, their size distribution was similar to that of very low density (S(f) 20-400) lipoprotein (VLDL) particles in plasma. After a fatty meal, jejunal absorptive cells and extracts of their homogenates contained lipid particles of VLDL-size as well as chylomicrons of various sizes. The percentage of triglyceride in isolated intestinal lipid particles increased during fat absorption. Our interpretation of these data is that chylomicrons are probably derived from intestinal lipoprotein particles by addition of triglyceride.

Dietary polyunsaturated fats of the W-6 and W-3 series reduce postprandial lipoprotein levels. Chronic and acute effects of fat saturation on postprandial lipoprotein metabolism.

The chronic and acute effects of different types of dietary fat on postprandial lipoprotein metabolism were studied in eight normolipidemic subjects. Each person was placed for 25 d on each of three isocaloric diets: a saturated fat (SFA), a w-6 polyunsaturated fat (w-6 PUFA) and a w-3 polyunsaturated fat (w-3 PUFA) diet. Two vitamin A-fat loading tests were done on each diet. The concentrations in total plasma and chylomicron (Sf greater than 1,000) and nonchylomicron (Sf less than 1,000) fractions of retinyl palmitate (RP) were measured for 12 h postprandially. Compared with the SFA diet, the w-6 PUFA diet reduced chylomicron and nonchylomicron RP levels 56 and 38%, respectively, and the w-3 PUFA diet reduced these levels 67 and 53%, respectively. On further analysis, the main determinant of postprandial lipoprotein levels was the type of fat that was chronically fed, which appeared to mediate its effect by changing the concentration of the endogenous competitor for the system that catabolizes triglyeride-rich lipoproteins. However, there was a significant effect of the acute dietary fat load, which appeared to be due to a differential susceptibility to lipolysis of chylomicrons produced by SFA as opposed to PUFA fat loads. The levels of postprandial lipoproteins are determined by the interaction of these chronic and acute effects.

Isolation of high density lipoproteins from rat intestinal epithelial cells.

Previous studies have defined forms of high density lipoproteins (HDL) in rat mesenteric lymph, suggesting that they have a secretory origin. This study describes the isolation and characterization of intestinal intracellular HDL. Two preparations were made as follows: (a) Rat enterocytes were isolated and a Golgi organelle fraction was prepared. (b) Cell homogenates were subjected to nitrogen cavitation and a cytoplasmic fraction was prepared. Lipoproteins were isolated from both preparations by sequential ultracentrifugation. When the HDL fraction (1.07-1.21 g/ml) was subjected to isopyknic density gradient ultracentrifugation, a peak of apoproteins A-I and B (apoA-I and apoB, respectively) was found at a density of 1.11-1.14 g/ml. Electron microscopy of the fraction showed spherical particles ranging in size from 6 to 13 nm. Immunoelectrophoresis revealed a precipitin arc in the alpha region against apoA-I which extended into the pre-beta region where a precipitin arc against apoB was also seen. ApoB antisera depleted the pre-beta particles whereas the alpha migrating particles remained. Lipid analysis of the whole HDL fraction revealed phospholipid, cholesteryl ester, and triglyceride as the major lipids. [3H]leucine was then administered into the duodenum and a radiolabeled intracellular HDL fraction was isolated. The newly synthesized apoproteins of the HDL fraction, as determined by gel electrophoresis, were apoB, apoA-I, and apolipoprotein A-IV (ApoA-IV). Immunoprecipitation of the apoB particles revealed apoA-I and apoA-IV in the supernatant. These data demonstrate that there are at least two intracellular intestinal forms of HDL particles, one of which contains apoB. The other particle contains apoA-I and apoA-IV, has alpha mobility, is spherical, and resembles a particle found in the lymph.

Evidence for the chylomicron origin of lipids accumulating in diabetic eruptive xanthomas: a correlative lipid biochemical, histochemical, and electron microscopic study.

Plasma lipoprotein alterations in nine insulin-dependent diabetics with hyperlipemia have been related to the lipid accumulating in eruptive xanthomas evolving in these patients. Histochemical and electron microscopic examination of xanthomas have been correlated with the lipid analyses in order to obtain additional evidence regarding the lipoprotein origin of lipids accumulating in the lesions. Both analytical and morphologic evidence suggested that circulating chylomicrons significantly contribute to the xanthoma lipids. All the patients had large quantities of circulating triglyceriderich chylomicrons which carried approximately 70% of the triglyceride found in the plasma. The fatty acid pattern of chylomicron and xanthoma triglycerides were similar. Triglyceride constituted the major lipid found in the xanthomas when they were sampled during their eruption. These findings, take in conjunction with histochemical and electron microscopic evidence of chylomicron particles in the dermal capillary walls, support the theory that blood lipoproteins, and particularly chylomicrons, permeated the vascular walls and the triglycerides carried by these lipoproteins apparently accumulated in tissue macrophages and perithelial cells which evolved into foam cells. Initiation of appropriate therapy resulted in clearance of the chylomicronemia and a concomitant resolution of the xanthomas as reflected by a decrease in total xanthoma lipid. Sequential studies of resolving xanthomas in five patients revealed that xanthoma triglyceride was mobilized more rapidly than cholesterol, resulting in a redistribution of the xanthoma lipids, so that the resolving lesions were cholesterol rich. Consistent with this change in lipid composition, correlative electron microscopy revealed loss of amorphous material from many of the foam cell vacuoles.

A genetic model for absent chylomicron formation: mice producing apolipoprotein B in the liver, but not in the intestine.

The formation of chylomicrons by the intestine is important for the absorption of dietary fats and fat-soluble vitamins (e.g., retinol, alpha-tocopherol). Apo B plays an essential structural role in the formation of chylomicrons in the intestine as well as the VLDL in the liver. We have developed genetically modified mice that express apo B in the liver but not in the intestine. By electron microscopy, the enterocytes of these mice lacked nascent chylomicrons in the endoplasmic reticulum and Golgi apparatus. Because these mice could not form chylomicrons, the intestinal villus enterocytes were massively engorged with fat, which was contained in cytosolic lipid droplets. These mice absorbed D-xylose normally, but there was virtually no absorption of retinol palmitate or cholesterol. The levels of alpha-tocopherol in the plasma were extremely low. Of note, the absence of chylomicron synthesis in the intestine did not appear to have a significant effect on the plasma levels of the apo B-containing lipoproteins produced by the liver. The mice lacking intestinal apo B expression represent the first genetic model of defective absorption of fats and fat-soluble vitamins and provide a useful animal model for studying nutrition and lipoprotein metabolism.

Systemic levels of carotenoids from mangoes and papaya consumed in three forms (juice, fresh and dry slice).

BACKGROUND: Vitamin A deficiency is a public health problem in Cameroon. Data on the bioavailability of carotenoid in fruits currently consumed in Cameroon are scarce. OBJECTIVE: To assess the systemic levels of carotenoids from mangoes and papaya consumed as juice, fresh or dried slices. METHODS: Two groups of seven healthy volunteers (24 and 25 years of age; body mass index: 21 and 22 kg/m(2) respectively for subjects fed mango and papaya), were submitted to three types of meal treatments (juice, fresh and dried fruit). On the experiment day, meals served to fasting subjects during breakfast, included bread, yogurt and one of the three forms of fruit. All the treatments lasted only one day during which blood samples were collected three times; during fasting (T(0)), 4 h (T(4)) and 8 h (T(8)) after the test meal. The carotenoids and retinol contents were analysed by high-performance liquid chromatography method. RESULTS: From the major carotenoids present in papaya and mangoes, lutein, alpha-carotene and beta-carotene were found in considerable amounts. Lycopene and cryptoxanthin that were the major carotenoids in papaya samples appeared in low amounts in the chylomicrons. Significant correlations were observed between these carotenoids (at T(0), T(4) and T(8)). The three forms of consumption contributed to the rise of serum retinol levels. A comparison between the three forms revealed that papaya and mangoes consumed in form of juice or fresh fruit are the best forms because they had higher bioavailability values. CONCLUSION: Association of these different forms of consumptions could lead to a better availability of these fruits throughout the year and therefore efficiently contribute to improve vitamin A status of the population.

Apolipoprotein E enrichment of immuno-separated chylomicron and chylomicron remnants following saturated fatty acids.

AIM: We examined the effect of meal fatty acids on lipid and apolipoprotein concentrations of very low density lipoprotein (VLDL) and chylomicron/chylomicron remnants in lipid fractions with a Svedberg flotation rate (Sf) 60-400 and Sf 20-60. METHODS AND RESULTS: Six healthy middle-aged men received in random order mixed meals enriched with saturated (SFA), polyunsaturated (PUFA) or monounsaturated (MUFA) fatty acids on 3 occasions. VLDL and chylomicron/chylomicron remnants in the lipid fractions were separated by immunoaffinity chromatography against apo B-100. In the Sf 60-400 chylomicron/chylomicron remnants, triacylglycerol and cholesterol concentrations were significantly lower following PUFA compared with SFA and MUFA (P < or = 0.05). Apolipoprotein (apo) E responses were significantly higher after SFA in chylomicron/chylomicron remnants and VLDL compared with PUFA and MUFA (P < 0.007). However, apo B responses (particle number) were higher following MUFA than SFA (P = 0.039 for chylomicron/chylomicron remnants). Composition of the chylomicron/chylomicron remnants (expressed per particle) revealed differences in their triacylglycerol and apo E contents; in the Sf 60-400 fraction, SFA-rich chylomicron/chylomicron remnants contained significantly more triacylglycerol than MUFA (P = 0.028), more apo E than PUFA- and MUFA-rich particles (P < 0.05) and in the Sf 20-60 fraction, more apo E than MUFA (P = 0.009). CONCLUSION: There are specific differences in the composition of chylomicron/chylomicron remnants formed after saturated compared with unsaturated fatty acid-rich meals which could determine their metabolic fate in the circulation and subsequent atherogenicity.

Distribution of apolipoproteins A-I and A-IV among lipoprotein classes in rat mesenteric lymph, fractionated by molecular sieve chromatography.

The distribution of apolipoproteins A-I and A-IV among lymph lipoprotein fractions was studied after separation by molecular sieve chromatography, avoiding any ultracentrifugation. Lymph was obtained from rats infused either with a glucose solution or with a triacylglycerol emulsion. Relative to glucose infusion, triacylglycerol infusion caused a 20-fold increase in the output of triacylglycerol, coupled with a 4-fold increase in output of apolipoprotein A-IV. The output of apolipoprotein A-I was only elevated 2-fold. Chromatography on 6% agarose showed that lymph apolipoproteins A-I and A-IV are present on triacylglycerol-rich particles and on particles of the size of HDL. In addition, apolipoprotein A-IV is also present as 'free' apolipoprotein A-IV. The increase in apolipoprotein A-I output is caused by a higher output of A-I associated with large chylomicrons only, while the increase in apolipoprotein A-IV output is reflected by an increased output in all lymph lipoprotein fractions, including lymph HDL and 'free' apolipoprotein A-IV. The increased level of 'free' A-IV, seen in fatty lymph, may contribute to, and at least partly explain, the high concentrations of 'free' apolipoprotein A-IV present in serum obtained from fed animals.

Hydrolysis of chylomicron polyenoic fatty acid esters with lipoprotein lipase and hepatic lipase.

The lipolysis of rat chylomicron polyenoic fatty acid esters with bovine milk lipoprotein lipase and human hepatic lipase was examined in vitro. Chylomicrons obtained after feeding fish oil or soy bean oil emulsions were used as substrates. The lipolysis was followed by gas chromatography or by using chylomicrons containing radioactive fatty acids. Lipoprotein lipase hydrolyzed eicosapentaenoic (20:5) and arachidonic acid (20:4) esters at a slower rate than the C14-C18 acid esters. More 20:5 and 20:4 thus accumulated in remaining tri- and diacylglycerols. Eicosatrienoic, docosatrienoic and docosahexanoic acids exhibited an intermediate lipolysis pattern. When added together with lipoprotein lipase, hepatic lipase increased the rate of lipolysis of 20:5 and 20:4 esters of both tri- and diacylglycerols. Addition of NaCl (final concentration 1 M) during the course of lipolysis inhibited lipoprotein lipase as well as the enhancing effect of hepatic lipase on triacylglycerol lipolysis. Hepatic lipase however, hydrolyzed diacylglycerol that had already been formed. Chylomicron 20:4 and 20:5 esters thus exhibit a relative resistance to lipoprotein lipase. It is suggested that the tri- and diacylglycerol species containing these fatty acids may accumulate at the surface of the remnant particles and act as substrate for hepatic lipase during a concerted action of this enzyme and lipoprotein lipase.

Triacylglycerol oxidation in pig lipoproteins after a diet rich in oxidized sunflower seed oil.

The effects of two sunflower seed oil diets differing in oxidation levels (PV in oils 1 and 190 mequiv O2/kg) on lipoprotein TAG and total lipid oxidation were investigated in growing pigs. For 2 wk, two groups of 10 pigs were fed either of the diets, after which blood samples were collected. A method based on RP-HPLC and electrospray ionization-MS was used for the analysis of oxidized TAG molecules in chylomicrons and VLDL. The baseline diene conjugation method was used for the estimation of in vivo levels of lipoprotein lipid oxidation. TAG molecules with a hydroxy, an epoxy, or a keto group attached to a FA, as well as TAG core aldehydes were detected in the samples. Typically, lipoprotein TAG and total lipids were more oxidized in the pigs fed on the oxidized oil compared with those fed on nonoxidized oil. Oxidation of dietary fat was thus reflected in the lipoprotein oxidation, which confirmed our earlier findings.

The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4.

We have identified a previously described 66K T4-binding protein as a lipoprotein composed of two molecules of apolipoprotein A-I, five of cholesteryl esters, nine of phosphatidylcholine, and two of sphingomyelin. This 68.4K high density lipoprotein (HDL) corresponds to the minor approximately 67K HDL subfraction that we recently demonstrated as binding most of the HDL-associated T4. Since we have recently found that lipids inhibit the binding of T4 to apolipoprotein A-I, the very low lipid content (16 mol/mol) of this 68K HDL relative to that (greater than 100 mol/mol) of high mol wt HDL subfractions may account for the preferential binding of T4 to the low mol wt subfraction.

Lipid domain in cancer cell plasma membrane shown by 1H NMR to be similar to a lipoprotein.

Human blood lipoproteins have been characterised by 1H NMR methods and chemical analysis, and comparisons made with the properties of the triglyceride-rich plasma membrane domain found in cancer cells. By means of selective and non-selective T1 experiments, the lipids in HDL and LDL are shown to be in diffusive exchange. In contrast, the lipids of chylomicra and VLDL do not exhibit lipid diffusion, and therefore resemble the neutral lipids of cancer cell plasma membranes. 2D scalar correlated NMR (COSY) spectra of cancer cells or solid tumours are similar to those obtained from VLDL and LDL. The long T2 relaxation value observed for neutral lipid methylenes in metastatic cancer cells (greater than 300 ms) was not observed for any of the 4 lipoproteins studied. None of the lipoprotein classes gave a T2 longer than 250 ms.

Composition of lymph chylomicrons from proximal or distal rat small intestine.

The composition of lymph chylomicrons secreted by rat proximal and distal small intestine were compared during constant perfusion of a lecithin-stabilized tri (1-14C) oleoyl glycerol emulsion, in pairs of unanesthesized rats with mesenteric lymph fistulas. By the 6th hr of infusion when 14C-triglyceride output was constant, the distal intestine secreted 33% less chylomicron phospholipid. Distal chylomicrons were larger and had higher triglyceride:phospholipid and higher apoprotein:phospholipid ratios than chylomicrons secreted by proximal intestine. The major apoprotein classes--apoB, apoA-I, apoE(= ARP), and C peptides--were present in both groups of chylomicrons, but in different proportions. Distal chylomicrons contained less apoA-I and more C peptides, with an increase in apoC-III3, and a decrease in apoC-III0, compared with proximal chylomicrons. The present study suggests that the distal intestine is defective in the utilization of phospholipid from the intestinal lumen for chylomicron phospholipid synthesis. Whether the observed changes in the size and phospholipid or apoprotein content of distal chylomicrons affect their system metabolism is presently not known.