Intravenous intralipid 10% vs. 20%, hyperlipidemia, and increase in lipoprotein X in humans.

To clarify the mechanisms of hyperlipidemia caused by infusion of Intralipid 10%, we compared lipoprotein metabolism during intravenous Intralipid 10% and Intralipid 20%, which contains only half the amount of egg yolk lecithin for the same content of triglyceride as Intralipid 10%. Ten patients receiving 20 ml.kg-1.day-1 of Intralipid 10% and 10 receiving 10 ml.kg-1.day-1 of Intralipid 20% were fed exclusively by total parenteral nutrition (TPN) providing 1.1 g amino acid and 30 kcal.kg-1.day-1 for 4-6 wk. Intravenous Intralipid 10% caused a marked increase in low-density lipoprotein (LDL), together with increases in phospholipid and cholesterol, especially free cholesterol. The progressive increase in lipoprotein X was in proportion with that of LDL or total lipid, whereas no increase in lipids, LDL, or lipoprotein X was observed during intravenous Intralipid 20%. A significant increase in apolipoproteins CIII and E with Intralipid 10% also caused a rise in lipoprotein X. With Intralipid 20%, however, the alterations in apolipoproteins were not observed. Lecithin:cholesterol acyltransferase (LCAT) activity was significantly elevated with Intralipid 10 but not 20%. Disappearance of lipoprotein X after cessation of Intralipid 10% was relatively rapid, and the half-life was 24-60 h. From these findings, the hyperlipidemia with Intralipid 10% was caused almost exclusively by the increase in lipoprotein X. The excess lecithin may be responsible for the formation of and increase in lipoprotein X. Furthermore, it was revealed that Intralipid 20% could be safely used without inducing hyperlipidemia.     

Alteration of lipoprotein profile during total parenteral nutrition with intralipid 10%

Eight patients were studied for lipoprotein profiles over a period of 3-7 weeks. Four patients received total parenteral nutrition (TPN), including 1000 ml/day of Intralipid 10%. Three patients received fat-free TPN, and one patient was tube fed 1000 ml/day of Intralipid 10% enterally. Fat-free TPN lowered plasma lipid, especially low density lipoprotein (LDL) and high density lipoproteins (HDL). On the other hand, intravenous administration of Intralipid 10% caused a marked increase of LDL, together with increases of phospholipid and cholesterol, especially free cholesterol. Triglyceride, VLDL, and HDL remained within the normal range in this group. Enteral administration of the same amount of Intralipid 10% did not cause a rise of LDL. Lipid composition of the increased LDL approximated that of lipoprotein X with the intravenous Intralipid 10%. From these findings, we suggest that phospholipids in Intralipid 10% formed abnormal LDL as the result of mobilization of cholesterol from extravascular tissues, when administered intravenously.     

Evidence that polyunsaturated lecithin induces a reduction in plasma cholesterol level and favorable changes in lipoprotein composition in hypercholesterolemic rats

For 30 d adult rats were fed a hypercholesterolemic (H) diet (25% saturated fat, 1% cholesterol and 0.5% cholic acid) containing different amounts of saponins (1% or 0.2%) and/or purified polyunsaturated lecithin (2.5% or 0.7%). Lecithin induced a striking reduction in the plasma levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. Saponins had only a very slight effect in lowering the level of VLDL cholesterol. Apoprotein A-I was unexpectedly present in VLDL, IDL and LDL after feeding rats the H diet and disappeared only after lecithin feeding. The activity of plasma lecithin-cholesterol acyltransferase was higher when the two lecithin diets were fed than when the other diets were fed. Fecal excretion of neutral sterols was unmodified by the various diets whereas acid steroid excretion increased after lecithin feeding. Saponins, when added with lecithin to the diet, reduced the beneficial effect of lecithin. The results indicate that polyunsaturated lecithin induced a reduction in plasma cholesterol, possibly through an increased formation of HDL particles.     

Increased frequency of icterus in parenterally fed patients after a change of lipid emulsion]

Parenteral nutrition is associated with liver enzyme abnormalities. Until 1993 the incidence of icterus was low in both academic hospitals in Amsterdam, the Netherlands (Academic Medical Centre (AMC) and Academic Hospital of the Free University (AZVU)). In 1993 Intralipid in the nutrition was replaced by Endolipid in the home total parenteral nutrition programme (AMC) and by Lipofundin S in AZVU. Fifty per cent of the patients in the home programme developed severe fatigue, jaundice and thrombocytopenia. These signs and symptoms disappeared over months when parenteral nutrition without fat was given. After reintroduction of Intralipid these signs and symptoms never recurred. In AZVU the incidence of jaundice increased from 21% in 1992 to 79% in 1993 (p = 0.0002). After reintroduction of Intralipid in 1994 the incidence of jaundice decreased to 16%. CONCLUSION: Although the lipid emulsions are equivalent according to the product specification, the described observation suggests that Lipofundin S and Endolipid cause more icterus than Intralipid, possibly caused bij an impurity in the fat emulsion.     

Short-term parenteral nutrition with glucose and Intralipid: effects on serum lipids and lipoproteins

We prospectively investigated the effect of a 3-wk course of parenteral nutrition with 20% glucose, 4.25% amino acids, and 10% Intralipid on plasma lipids and lipoproteins in a cohort of 12 nutritionally replete patients with inflammatory bowel disease. Mean total serum cholesterol and mean total serum phospholipids increased in parallel throughout the study; density gradient ultracentrifugation demonstrated these increases were due to the appearance of lipoprotein-X. The mean low-density lipoprotein (LDL) mass on the density gradients decreased during the study and high-density lipoprotein (HDL) cholesterol levels decreased by 28% by the end of the third week. Plasma free fatty acids decreased by 42%. These results demonstrate that the glucose and 10% Intralipid regimen caused modest decreases in serum HDL cholesterol and LDL mass and the prompt appearance of lipoprotein-X with attendant hypercholesterolemia and hyperphospholipidemia. Patients undergoing long-term treatment with glucose and Intralipid should be closely monitored for the occurrence of significant dyslipoproteinemia.     

Replacement of dietary fat with palm oil: effect on human serum lipids, lipoproteins and apolipoproteins.

Thirty-eight male volunteers participated in a double-blind cross-over trial evaluating the effect of replacing the usual sources of saturated fat in the Dutch diet (animal fats and hydrogenated oils) by palm oil, which is virtually free of cholesterol and trans-fatty acids, on serum lipids, lipoproteins and apolipoproteins. Maximum (about 70%) replacement had no significant effect on serum total cholesterol or most lipoprotein fractions, but resulted in an 11% increase in serum high-density-lipoprotein (HDL)2-cholesterol relative to the control (P2 = 0.01). The palm-oil diet also caused an 8% decrease in low-density-lipoprotein (LDL):HDL2 + HDL3-cholesterol ratio (P2 = 0.02) as well as a 9% decrease in triacylglycerols in the low-density-lipoprotein fractions (P2 = 0.01). Palm oil consumption resulted in a 4% increase in serum apolipoprotein AI (P2 = 0.008) and a 4% decrease in apolipoprotein B (P2 = 0.01) relative to the control diet; the B:AI apolipoprotein ratio was decreased by 8% (P2 < 0.0001). These results were not significantly affected by the different lipoprotein E phenotypes of the volunteers. Although the observed differences were relatively modest, the present study, nonetheless, indicates that dietary palm oil, when replacing a major part of the normal fat content in a Dutch diet, may slightly reduce the lipoprotein- and apolipoprotein-associated cardiovascular risk profiles.     

Increased lipoprotein X causes hyperlipidemia during intravenous administration of 10% fat emulsion in man

To clarify the mechanisms of hyperlipidemia during intravenous Intralipid 10%, lipoprotein profiles including lipoprotein X were studied in 13 patients receiving 2.0 g of fat per kilogram per day by Intralipid 10% over a period of 8 weeks. All patients were fed exclusively by total parenteral nutrition providing 1.1 g of amino acid and 30 kcal/kg per day. Intravenous administration of Intralipid 10% caused a marked increase of low-density lipoprotein (LDL), phospholipid, and cholesterol, especially free cholesterol, whereas triglyceride, very-low-density lipoprotein, and high-density lipoprotein remained within the normal range. Lipid composition of LDL approximated that of lipoprotein X progressively with the intravenous Intralipid 10%. Quantification of lipoprotein X revealed that its increase was proportionate with that of LDL and total lipid. From these findings, hyperlipidemia during intravenous Intralipid 10% is induced almost exclusively by the increased lipoprotein X.     

Plasma activities of lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase in patients considered for parenteral nutrition with fat emulsion

Intralipid is a fat emulsion which is widely used for intravenous nutrition in very ill patients. In order to know more about the capacity of these patients to metabolize exogenous triglycerides, the plasma activities of lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT), the key enzymes in the metabolism of serum lipoproteins were measured by a radioisotope technique in 23 critically ill patients and 20 patients with recent major surgery. Compared with normal volunteers, the activities were significantly decreased. On the other hand, the capacity to clear intravenously given Intralipid (0.1 g/kg), expressed as fractional removal rate (K2), was retained in patients. It is suggested that the measurement of K2 could not be useful to evaluate the capacity of Intralipid administration to satisfy the metabolic needs and also that its utilization must be reevaluated in terms of potential harmful effects.     

Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--changes in serum concentrations and distributions of apolipoproteins A-I, A-IV and E

The effects of a high-fat and high-cholesterol diet (HFC diet) on serum lipoproteins and apolipoproteins were studied in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY). In particular, the changes in serum concentrations and distributions among lipoprotein fractions of apolipoproteins A-I, A-IV and E (apo A-I, A-IV and E) were investigated in detail. These apolipoproteins are the main protein constituents of high density lipoprotein (HDL) which is considered to be an anti-atherogenic factor and accounts for a large part of the serum lipoproteins in the rat. Serum lipoprotein fractions were isolated by stepwise density-gradient ultracentrifugation. The alterations in lipoprotein fractions and apolipoproteins in lipoprotein fractions were roughly estimated by native gradient polyacrylamide gel electrophoresis and sodium dodecyl sulfate (SDS)-gradient polyacrylamide gel electrophoresis. Next, the concentrations of apo A-I, A-IV and E in serum, serum lipoprotein fractions and serum lipoprotein-free fraction were measured by rocket immunoelectrophoresis according to the method of Laurell as modified by us. Cholesterol was enzymatically determined by a commercially available kit. The results obtained were as follows: 1) A remarkable increase in the very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) fractions was observed in WKY and SHRSP. This was associated with a remarkable increase in the cholesterol and apo B contents and with a significant increase in the apo E content. These changes in the VLDL and IDL fractions were more drastic in SHRSP than in WKY, which suggests the promotive effect of hypertension in SHRSP on the production of VLDL and IDL fractions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term effects of vasectomy: Part I: Biochemical parameters

Two-hundred-sixty vasectomized industrial workers were randomly selected for the study group. An equal number of industrial workers were taken as matched controls. The results indicated that there was a decrease in the total low density lipoprotein (LDL) cholesterol and an increase in the high density lipoprotein (HDL) cholesterol, whereas triglycerides remained unchanged. The findings of the lipoprotein fractions corroborated well with the lipid parameters. Glucose level showed a significant decrease in the study group whereas uric acid levels remained unchanged. All the changes observed in biochemical parameters mentioned here were within the normal range. The percentage of abnormal electrocardiograms (ECG) did not show any difference between the 2 groups. Hence no adverse effects were noticed in any of the parameters studied following vasectomy.     

Tracking of serum lipids and lipoproteins from childhood to adulthood. The Bogalusa Heart Study

Serum lipids (total cholesterol and triglycerides) and lipoprotein cholesterol fractions (low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and high density lipoprotein (HDL) cholesterol) have been measured approximately every 3 years on children and young adults since 1973-1974 in Bogalusa, Louisiana, a community of approximately 22,000 individuals, one-third of whom are black and two-thirds of whom are white. A total of 1,586 children were examined both at baseline (1973-1974) and at the most recent survey (1984-1986), providing 12 years of follow-up. The decreases in levels noted during puberty for total cholesterol and LDL cholesterol, primarily for boys, were followed by a rise until age 26 years. HDL cholesterol levels, particularly for white boys, continued to drop after age 14 years, yielding increasingly high LDL cholesterol/HDL cholesterol ratios. Tracking, as measured by both correlation coefficients and persistence at extreme quartiles, was evident for all of the lipids and lipoproteins. The 12-year correlation coefficients were greatest for LDL cholesterol and no trend in the magnitude of the correlation coefficients with age was noted. Tracking for HDL cholesterol was better after age 9 years, particularly for white males. Approximately 50% of those children who had total cholesterol levels or LDL cholesterol levels above the 75th percentile at baseline remained elevated 12 years later. For HDL cholesterol, a trend with age was noted for white boys: 42% of those aged 9-14 years in the lower most quartile persisted in this rank 12 years later. The best predictor of follow-up lipid or lipoprotein level was baseline level. The next best predictor was increase in weight as defined by weight/height, an index of obesity. That serum lipid and lipoprotein levels continue to track from childhood into young adulthood points to the necessity of measurement early in life and, where indicated, the introduction of preventive and interventional programs aimed at developing healthy lifestyles.     

5种植物油对大鼠血脂和脂质过氧化的影响

观察 5种植物油在高脂血症形成过程中对大鼠血脂和脂质过氧化的影响。在高脂饲料中分别加入6 %的猪油、松籽油、紫苏油、黑加仑油、琉璃苣油和月见草油喂饲 Wistar雄性成年大鼠 3周 ,5种植物油组大鼠血清甘油三酯 (TG)、总胆固醇 (TC)、低密度脂蛋白胆固醇 (L DL- C)、L DL- C与高密度脂蛋白胆固醇(HDL - C)比值 (L DL - C/ HDL - C)的增加值和 HDL - C/ TC、卵磷脂胆固醇酰基转移酶 (L CAT)活性的下降均不同程度地低于单纯食猪油的高脂对照组。紫苏油、黑加仑油、琉璃苣油和月见草油可提高血清 HDL- C、高密度脂蛋白亚组分 胆固醇 (HDL2 - C)及 HDL2 - C与高密度脂蛋白亚组分 胆固醇 (HDL3- C)比值 (HDL2 - C/ HDL3- C)。紫苏油、黑加仑油和月见草油组大鼠肝脏过氧化脂质 (L PO)含量高于松籽油、琉璃苣油和猪油组。结果表明 5种植物油均具有一定的调节血脂作用 ,松籽油和琉璃苣油的组织脂质过氧化物相对较低     

Effects of vitamin E deficiency on the distribution of cholesterol in plasma lipoproteins and the activity of cholesterol 7 alpha-hydroxylase in rabbit liver

Vitamin E-deficient rabbits with signs of muscular dystrophy showed accumulation of cholesterol in muscle as well as elevation of plasma cholesterol. The increase in plasma cholesterol was detected in low density lipoprotein (LDL) and very low density lipoprotein (VLDL) but not in high density lipoprotein (HDL) fractions of plasma lipoproteins. In liver, the activity of cholesterol 7 alpha-hydroxylase, the key enzyme involved in degradation of cholesterol, was approximately one-fifth that of control rabbits. Cytochrome P-450 level of liver microsomes was also reduced significantly. These results suggested that accumulation of cholesterol observed in dystrophic muscle of vitamin E-deficient rabbits may be due to an increase in LDL and VLDL cholesterol, the plasma lipoproteins carrying cholesterol to peripheral tissue, and to a decrease in cholesterol 7 alpha-hydroxylase activity, whose activity may have been affected by the reduced level of cytochrome P-450.     

Metabolic syndrome and renal failure: similarities and differences

The metabolic syndrome (MS) and chronic kidney disease (CKD) share many similar risk factors for cardiovascular disease. Both are associated with increased triglyceride (TG) levels, both associated with increased small dense low density lipoprotein (LDL), both with decreased high density lipoprotein (HDL) levels. In both cases HDL particle size is reduced. The TG content of HDL and very low density lipoprotein (VLDL) and remnants are increased, resulting in a dyslipidemia. Both are associated with increased inflammation, a hypercoagulable state and insulin resistance. Establishing whether these similarities are the result of identical biological processes or instead represent similar end results of different processes is further confounded by the associated both of adiposity and of MS with the incidence and progression of renal failure. Differences are present however. In MS hepatic VLDL synthesis is increased driven by increased flux of free fatty acids from muscle, adipose tissue and gut to the liver. VLDL is catabolized to LDL and the transfer of TG to HDL by cholesterol ester transfer protein destabilizes HDL leading to its rapid clearance. In CKD HDL fails to mature due to reduced activity of lecithin cholesterol transfer protein. In MS inflammation primarily arises from increased visceral adipose tissue, while inflammation is largely unrelated to body composition in CKD. Increased production of TG rich lipoproteins predominates in MS, while decreased disposal of TG rich proteins predominates as the cause of increased TG levels in CKD. Whether treatment of elements of MS, with the exception of hypertension, will avoid the onset and progression of renal failure is unknown.     

Distribution of PCB Congeners, DDE, Hexachlorobenzene, and Methylsulfonyl Metabolites of PCB and DDE Among Various Fractions of Human Blood Plasma

The concentrations of chlorinated biphenyls (CBs), 1,1-bis(4-chlorophenyl)-2,2-dichloroethene (DDE), hexachlorobenzene (HCB), and the methylsulfonyl metabolites of CBs (MeSO₂-CBs) and DDE (MeSO₂-DDE) were determined in human plasma samples and in the fractions obtained by ultracentrifugation of plasma into very-low-density (VLDL), low-density (LDL), high-density (HDL) lipoprotein and lipoprotein depleted (LPDP) fractions (containing primarily albumin). The concentrations of triacylglycerols, cholesterol, phospholipids, and apolipoprotein B (apoB) were determined. The organochlorine compounds were associated with all fractions, but predominantly with the LPDP fraction. On an average 44% of CBs, 61% of MeSO₂-CBs, 73% of DDE, 77% of MeSO₂-DDE, and 45% of HCB were distributed in the LPDP fraction. A tendency to greater association of 3-methylsulfonyl substituted than of corresponding 4-methylsulfonyl substituted chlorobiphenyls to the LPDP fraction was noticed. Among the lipoprotein fractions, LDL was the main carrier of HCB, DDE and CBs. MeSO₂-DDE was predominantly found in HDL and MeSO₂-CBs were distributed equally among the LDL and HDL fractions. Calculating the concentrations of organochlorine compounds in relation to the content of apoB, the levels were about 10 times higher in VLDL than in LDL. Received: 24 April 1998/Accepted: 24 April 1999     

Dietary protein level and origin (casein and highly purified soybean protein) affect hepatic storage, plasma lipid transport, and antioxidative defense status in the rat

The effects of different proportions (10, 20, and 30%) of dietary casein or highly purified soybean protein on lipid metabolism were studied in growing Wistar rats. Hepatic, plasma and lipoprotein lipid, and protein concentrations, plasma thiobarbituric acid-reactive substance (TBARS) levels, and resistance of red blood cells against free-radical attack were determined after a 4-wk dietary regimen. Compared with the 20% casein diet, the 20% soybean protein diet exhibited similar cholesterolemia but lower plasma triacylglycerol concentrations and very-low-density lipoprotein (VLDL) particle number, as measured by diminished contents of VLDL-triacylglycerol, VLDL-protein, and VLDL-apolipoprotein (Apo) B (B-100 and B-48). The soybean protein diet raised high-density lipoprotein (HDL)(2-3) particle number, as measured by enhanced concentrations of HDL(2-3) cholesterol, HDL-phospholipid, and HDL-ApoA-I. Increasing casein or soybean protein level (from 10 to 30%) in the diet involved higher VLDL-ApoB (B-100 and B-48), indicating an increase in the number of VLDL particles. Feeding the 30% casein or 30% soybean protein diet enhanced LDL-HDL(1) cholesterol contents. Despite similar HDL(2-3)-ApoA-I levels, the 30% casein diet enhanced the HDL(2-3) mass and its cholesterol concentrations. In contrast, feeding either the 10 or 30% soybean protein diet significantly lowered HDL(2-3) cholesterol and ApoA-I levels. These effects on cholesterol distribution in lipoprotein fractions occurred despite unchanged total cholesterol concentrations in plasma. Feeding 20% soybean protein versus 20% casein involved lower plasma TBARS concentrations. Decreasing casein or soybean protein levels in the diet were associated with higher plasma TBARS concentrations and had a lower resistance of red blood cells against free-radical attack. The present study shows that dietary protein level and origin play an important role in lipoprotein metabolism and the antioxidative defense status but do not affect total cholesterol concentrations in plasma.     

Effects of guar gum on plasma lipoproteins and apolipoproteins C-II and C-III in patients affected by familial combined hyperlipoproteinemia

In recent years, guar gum has been shown to be a potent hypocholesterolemic agent. The effects of this fiber on triglycerides are less clear. In order to evaluate the influence of guar supplementation on plasma lipoproteins and apolipoprotein C-II (apoC-II) and apolipoprotein C-III (apoC-III) isoforms (apoC-III2, apoC-III1, apoC-III0), 16 g/day of guar gum were administered to 12 outpatients affected by familial combined hyperlipoproteinemia for a period of 60 days. Mean total cholesterol and triglyceride levels significantly decreased after 15 days of treatment and persisted reduced at the 30th and 60th day of guar supplementation. While low-density lipoprotein cholesterol paralleled the reduction of total plasma cholesterol, we did not observe any change in the cholesterol content of high-density lipoprotein (HDL) subfractions (HDL2 and HDL3) during the study. A redistribution of the relative content of very low-density lipoprotein apoC-III isoforms with a significant increase of apoC-III1 and a decrease of apoC-III0 was observed after 15, 30, and 60 days of guar gum administration. The results show that guar gum reduces not only cholesterol but also triglyceride levels in patients affected by familial combined hyperlipoproteinemia. Further studies are needed to confirm the suggestion that the different distribution of very low-density lipoprotein apoC-III isoforms induced by guar supplementation may influence the behavior of plasma triglycerides.     

Tocopherol distribution in serum lipoproteins with respect to red blood cell tocopherol levels in children

The relation of lipoprotein tocopherol levels to red blood cell (RBC) tocopherol was investigated in 81 healthy children, comprising 44 males and 37 females, using a new technique for separation of individual lipoprotein fractions. 1. In children there were no age and sex differences in tocopherol contents among individual lipoprotein fractions. The tocopherol content of high density lipoprotein (HDL) was slightly higher than that of low density lipoprotein (LDL), but this difference was not statistically significant. 2. The tocopherol content of HDL fractions was closely correlated with RBC tocopherol concentration, but there was no relationship in tocopherol levels between RBC and LDL and between RBC and very low density lipoprotein (VLDL). 3. There were no age and sex differences in contents of total cholesterol (T-ch), triglycerides (TG), phospholipids (PL), total lipids, HDL-cholesterol, LDL or VLDL in children.     

Postprandial changes in the plasma concentration of alpha- and gamma-tocopherol in human subjects fed a fat-rich meal supplemented with fat-soluble vitamins

The plasma concentrations of alpha (alpha)- and gamma (gamma)-tocopherol in 10 male and 15 female subjects (n = 14) received 1 g fat/kg body wt as soybean oil, and the meal was supplemented with 100% of the RDA for fat-soluble vitamins. In expt. 2, the subjects (n = 11) received 1 g fat/kg body wt as 50% soybean oil + 50% cream, and the meal was supplemented with 200% of the RDA for fat-soluble vitamins. The ratio of gamma- :alpha-tocopherol given in the test meal of expt. 1 was 2.8:1 and in expt. 2 was 0.9:1. Blood samples were obtained 0, 3, 6, 9 and 12 h after the meal. Tocopherol concentration was measured in plasma and lipoprotein fractions. In both studies, plasma triglyceride concentration increased significantly after the meal (P less than 0.001). Mean plasma cholesterol and alpha-tocopherol concentrations were unchanged, but plasma gamma-tocopherol concentration was significantly increased at 6, 9 and 12 h after the meal (P less than 0.05). The increase in plasma gamma-tocopherol was due to increases within the triglyceride-rich lipoprotein (TRL) fraction (d less than 1.006 g/ml) at earlier timepoints, followed by a sustained increase within low density lipoprotein (LDL) and high density lipoprotein (HDL) fractions at later timepoints. In contrast, alpha-tocopherol in LDL and HDL decreased postprandially, concomitant with a rise in TRL alpha-tocopherol. Our results are consistent with the concept that there are differences in the distribution of alpha- and gamma-tocopherol in postprandial lipoproteins.     

Sex differences in high-density lipoprotein cholesterol and subfractions among young black adults

The high-density lipoprotein cholesterol and high-density lipoprotein subfraction (HDL2 and HDL3) concentrations were examined in 170 young black adults. The women examined had significantly higher total high-density lipoprotein cholesterol concentrations than the men, i.e., 57.0 mg/dl vs 51.2 mg/dl, P less than 0.002. The increased high-density lipoprotein cholesterol among women represented a significant increase in both HDL2 and HDL3 cholesterol concentrations. The sex differential could not be explained by body mass index, alcohol consumption, or physical activity. The determinants of high-density lipoprotein cholesterol for men appeared to be different than those for women.