In vitro transfer of apolipoproteins from plasma lipoproteins to artificial lipid particles

Our earlier studies in vivo revealed that artificial lipid particles (exo TG) in lipid emulsion acquire apolipoprotein C-II (apo C-II) from high density lipoprotein (HDL). Since the transfer of apo C-II to exo TG terminated within a short time after the intravenous injection of exo TG, it is likely that exo TG has a high affinity for apolipoprotein. This hypothesis has been investigated in vitro. Human plasma was incubated at 37 degrees C with or without a 10% emulsion of soybean oil for 5 min and 60 min. After the incubation, the plasma was separated into HDL, low density lipoprotein (LDL) and very low density lipoprotein (VLDL). Levels of apo C-II, C-III and E in each lipoprotein fraction were quantified. When the plasma was incubated without exo TG, the distribution of apo C-II and C-III in the lipoprotein fractions was unchanged after incubations for 5 and 60 min. However, when the plasma was incubated with exo TG, apo C-II and C-III in the HDL fraction decreased after a 5 min incubation, while those in the VLDL fraction increased. Apo E in each lipoprotein fraction did not change after 5- and 60-min incubations regardless of the presence or absence of exo TG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Capacity of high-density lipoprotein for donating apolipoproteins to fat particles in hypertriglyceridemia induced by fat infusion.

Acquisition of apolipoproteins C-II (apoCII) and C-III (apoCIII) is essential for the regulation of intravascular metabolism of fat particles (exoTG). This study was undertaken to investigate whether the capacity of high-density lipoprotein (HDL) for donating apoCII and apoCIII is influenced by the concentration of triglycerides (TGs) in plasma. A fat emulsion was infused into six male volunteers at a rate of 0.5 g TG.kg-1.h-1 (priming dose) for 30 min. For the following 160 min, fat was infused a fat emulsion was infused into the same subjects at a rate of 0.3 g.kg-1.h-1 for 160 min after the administration of the priming dose of fat emulsion for 30 min (experiment 2). The plasma TG concentrations and the amounts of apoCII and apoCIII in exo TG and HDL were monitored. The concentration of TG in the plasma stabilized at approximately 500 mg/dl in experiment 1, whereas it continued to increase to 815 +/- 42 mg/dl at 160 min after the start of the infusion of the fat emulsion in experiment 2. In experiment 1, the amount of both apoCII and apoCIII began to increase in exoTG and to decrease in HDL after the initiation of fat infusion. These changes in the distribution of apoC stabilized while the TG concentration remained at a plateau value. However, in experiment 2, the amount of apoC in exoTG did not increase further in response to the additional rise in plasma TG level. These results suggest that there is a relative lack of apoC that can be donated by HDL, depending on the quantitative balance between exoTG and HDL.(ABSTRACT TRUNCATED AT 250 WORDS)     

Apolipoprotein C-II modifications associated with an infusion of artificial lipid particles

Artificial lipid particles used as parenteral nutrition solution do not contain any apolipoproteins when they are infused into the circulation. Despite the absence of apolipoproteins, the metabolism of artificial lipid particles is similar to that of chylomicrons which contain various kinds of apolipoprotein. Of the known apolipoproteins, apolipoprotein C-II (apo C-II) is important in the hydrolysis of triglyceride-rich lipoproteins via involvement in the activation of lipoprotein lipase. Modifications of apo C-II associated with intravenous infusion of a lipid emulsion were investigated in eight patients. Changes in apo C-IIs in high density lipoproteins (HDL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) together with the plasma level of triglycerides, were quantified before and for 90 min after a bolus injection of a 10% lipid emulsion (1 ml/kg of body weight). Immediately prior to the injection, 54% of the total amount of apo C-II was present in HDL, while 27% was present in VLDL. After 5 to 10 min, the amount of apo C-II in HDL decreased to 29% of the total, while that in VLDL increased to 62%. Subsequently, the amounts of apo C-II in HDL and VLDL began to return to the preinjection levels. These variations in apo C-II were closely correlated with the plasma clearance of triglyceride. The result indicates that the injected lipids are not inert particles during their short intravascular life, but that they acquire apo C-II from HDL.     

Arterial deepvenous difference of lipoproteins in skeletal muscle of patients in postoperative state: effects of medium chain triglyceride emulsion

The effect of fat infusion with medium chain triglycerides (MCT) and long chain triglycerides (LCT) on serum lipoproteins before and after passage through the skeletal muscle was investigated with the forearm technic in eight patients after abdominal operation. All lipoprotein fractions were enriched with triglycerides and phospholipids from infused artificial fat particles with the consequence of significantly increased ratios of TG/PL and TG/apo B in VLDL, of TG/apo B in LDL and TG/apo A-I in HDL. Uptake and release of lipoprotein components by skeletal muscle are given by arterial-deepvenous differences considering the blood flow rates. The positive arterial-deepvenous difference of VLDL triglycerides after 4-hr infusion is interpreted as cleavage and uptake of infused MCT by the muscle. The release of LDL is more pronounced after the fat infusion than before, suggesting a degradation and enhanced catabolism of artificial fat particles. HDL release may be also a consequence of catabolism of artificial TG/PL-particles. These results indicate an uptake of MCT/LCT emulsion by the skeletal muscle.     

Effect of protein, unsaturated fat, and carbohydrate intakes on plasma apolipoprotein B and VLDL and LDL containing apolipoprotein C-III: results from the OmniHeart Trial

BACKGROUND: Plasma apolipoprotein B (apo B) and VLDL and LDL with apolipoprotein C-III (apo C-III) are independent risk factors for cardiovascular disease (CVD). Dietary intake affects lipoprotein concentration and composition related to those apolipoproteins. OBJECTIVE: We studied differences in apo B lipoproteins with and without apo C-III after 3 healthy diets based on the Dietary Approaches to Stop Hypertension Trial diet. DESIGN: Healthy participants (n = 162) were fed each of 3 healthy diets for 6 wk in a crossover design. Diets differed by emphasis of either carbohydrate (Carb), unsaturated fat (Unsat), or protein (Prot). Blood was collected at baseline and after diets for analysis. RESULTS: Compared with the Carb diet, the Prot diet reduced plasma apo B and triglycerides in VLDL with apo C-III (16%, P = 0.07; 11%, P = 0.05, respectively) and apo B in LDL with apo C-III (16%, P = 0.04). Compared with the Unsat diet, the Prot diet reduced triglycerides in VLDL with apo C-III (16%, P = 0.02). Compared with baseline (subjects' usual diet was higher in saturated fat), the Prot diet reduced apo B in LDL with apo C-III (11%, P = 0.05), and all 3 diets reduced plasma total apo B (6-10%, P < 0.05) and apo B in the major type of LDL, LDL without apo C-III (8-10%, P < 0.01). All 3 diets reduced the ratio of apo C-III to apo E in VLDL. CONCLUSIONS: Substituting protein for carbohydrate in the context of a healthy dietary pattern reduced atherogenic apo C-III-containing LDL and its precursor, apo C-III-containing VLDL, resulting in the most favorable profile of apo B lipoproteins. In addition, compared with a typical high-saturated fat diet, healthy diets that emphasize carbohydrate, protein, or unsaturated fat reduce plasma total and LDL apo B and produce a lower more metabolically favorable ratio of apo C-III to apo E.     

Serum lipoprotein changes after prolonged intralipid infusion in malnourished haemodialysis patients

Fat emulsions have been shown to be on efficient source of energy support in malnourished haemodialysis patients. This work was conducted in order to study the effect of prolonged intralipid infusion, during dialysis, on lipid metabolism. The following fasting serum parameters were measured before and after a 1 month infusion of 20% Intralipid (67 kJ/kg body wt/dialysis) in 10 malnourished patients undergoing dialysis: total cholesterol, triglycerides, phospholipids, HDL-cholesterol, LDL-cholesterol, HDL2-cholesterol, HDL3-cholesterol, apolipoproteins A-I, A-II, A-IV, C-II, C-III, and lipoproteins A-I, A-I A-II, EB and (a). After prolonged lipid infusion, the apoprotein B (p < 0.05) and C-II (p < 0.005) increased suggesting a triglyceride transport activation. Apolipoprotein A-I (p < 0.05) and lipoprotein A-I (p < 0.05) decreased without a change in total cholesterol. Lipoprotein (a) decreased in each case (p < 0.005), suggesting a reduction of its related risk of atherogenesis.     

Increased plasma concentrations of lipoprotein(a) during a low-fat, high-carbohydrate diet are associated with increased plasma concentrations of apolipoprotein C-III bound to apolipoprotein B-containing lipoproteins

BACKGROUND: Low-fat, high-carbohydrate (LFHC) diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)] and of triacylglycerol- rich lipoproteins (TRLs). OBJECTIVE: We tested whether increases in plasma Lp(a) induced by an LFHC diet are related to changes in TRLs. DESIGN: Healthy men (study 1; n = 140) consumed for 4 wk each a high-fat, low-carbohydrate diet (HFLC; 40% fat, 45% carbohydrate) and an LFHC diet (20% fat, 65% carbohydrate). Plasma lipids; lipoproteins; apolipoprotein (apo) B, A-I, and C-III; and Lp(a) were measured at the end of each diet. In a second group of men following a similar dietary protocol (study 2; n = 33), we isolated apo(a)-containing particles by immunoaffinity chromatography and determined the concentrations of apo C-III in ultracentrifugally isolated subfractions of apo B-containing lipoproteins. RESULTS: In study 1, plasma concentrations of Lp(a) (P < 0.001), triacylglycerol (P < 0.001), apo B (P < 0.005), apo C-III (P < 0.005), and apo C-III in apo B-containing lipoproteins (non-HDL apo C-III) (P < 0.001) were significantly higher with the LFHC diet than with the HFLC diet. Stepwise multiple linear regression analysis showed that the association of changes in Lp(a) with changes in non-HDL apo C-III was independent of changes in body mass index, apo B, LDL cholesterol, and HDL cholesterol. Plasma lipid and lipoprotein changes were similar in study 2, and we found that both total apo C-III and the apo C-III content of apo(a)-containing particles were increased in a TRL fraction consisting predominantly of large VLDL particles [TRL-apo(a)]. CONCLUSIONS: The increase in plasma Lp(a) with an LFHC diet is significantly associated with an increase in non-HDL apo C-III. Enrichment of TRL-apo(a) with apo C-III may contribute to this dietary effect on Lp(a) concentrations.     

Heritability of Serum Apolipoprotein Concentrations in Middle-Aged Japanese Twins

Background

Studies of the genetic and environmental influences on apolipoproteins have been conducted, but few have used data from Japanese twins. The aim of this study was to quantify and compare the genetic and environmental causes of individual differences in the serum concentrations of apolipoproteins in Japanese middle-aged twins.

Methods

Apo A-I, apo A-II, apo B, apo C-II, apo C-III, and apo E were studied. A total of 142 twin pairs, aged 45 through 65 years, were enrolled: 85 monozygotic pairs (59 male, 26 female) and 57 same-sexed dizygotic pairs (43 male, 14 female). The intraclass correlation coefficient and structural equation modeling were used to estimate the best-fitting model and heritability.

Results

Sixteen percent to 75% of the total variances of apo A-I, apo C-II, and apo C-III were attributable to genetic influence; apo A-I and apo C-II were influenced by dominant genetic factors. Twenty percent to 73% of the total variances of apo A-II, apo B, and apo E were attributable to additive genetic influence; apo B was clearly influenced by common environmental factors. Furthermore, the heritability of all apolipoproteins was higher among females than among males.

Conclusions

Genetic factors, including additive genetic effects (A) and dominant effects (D), influence apolipoprotein levels. However, a common environment does not influence the variances of these apolipoproteins, with the exception of apo B. Furthermore, the heritability of apolipoprotein phenotypes differs by sex.Key words: apolipoprotein, heritability, adult twins     

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.     

Dietary monounsaturated fat activates metabolic pathways for triglyceride-rich lipoproteins that involve apolipoproteins E and C-III

BACKGROUND: Dietary monounsaturated fat (MUFA) and complex carbohydrates have different effects on triglyceride-rich lipoprotein (TRL) metabolism. OBJECTIVE: We hypothesized that apolipoprotein (apo) E and apo C-III might be involved in these dietary effects because of their crucial role in TRL metabolism. DESIGN: Twelve adults consumed, for 3 wk each, 2 isocaloric diets: first a carbohydrate-rich diet (48% complex carbohydrate, 8% MUFAs) and then a MUFA-rich diet (31% complex carbohydrate, 24% MUFAs) 12 mo later. The dietary composition of other macronutrients in the 2 diets was similar. Body weight was kept constant. Postprandial apo B kinetic studies using stable-isotope tracers were performed after each dietary intervention. Multiple VLDL, intermediate-density lipoprotein (IDL), and LDL fractions were prepared on the basis of apo E and apo C-III contents. RESULTS: The MUFA diet increased by approximately 4-6-fold, the secretion of VLDLs and IDLs containing both apo E and apo C-III (E+CIII+) (P < 0.05). These are TRLs that mostly cleared from the circulation and are minor precursors of LDL. The MUFA diet also decreased by 60% (P < 0.05) the secretion of the TRLs without apo E or apo C-III (major precursors of LDL in plasma) and decreased their flux to LDLs. Total LDL flux did not change because the MUFA diet increased the flux to LDL from E-CIII+ TRLs, a process that requires the removal of apo C-III. In addition, the MUFA diet significantly increased the TRL fractional catabolic rate by 50% and doubled the percentage of TRLs that were cleared rather than being converted to LDLs. CONCLUSION: MUFA intake activates synthetic and rapid catabolic pathways for TRL metabolism that involve apo E and apo C-III and suppresses the metabolism of more slowly metabolized VLDLs and IDLs, which do not contain these apolipoproteins.     

Glucosyl hesperidin lowers serum triglyceride level in hypertriglyceridemic subjects through the improvement of very low-density lipoprotein metabolic abnormality

To examine the serum triglyceride (TG)-lowering effect of a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), and its mechanisms, we carried out a G-hesperidin administration test in hypertriglyceridemic subjects. G-Hesperidin was administered to the subjects at 500 mg/d for 24 wk. In this study, the subjects were classified into high-TG type (TG > 150 mg/dL), borderline-TG type (TG 110-150 mg/dL) and normal-TG type (TG < 110 mg/dL) on the basis of their initial serum TG values. Among these phenotypes, serum TG level significantly decreased in the high-TG type during the G-hesperidin administration period. It was also observed that elevated values of serum remnant-like particle cholesterol (RLP-C), apolipoprotein (apo) B, apo C-II, apo C-III and apo E occurred in the high-TG type and that these serum levels were significantly reduced by G-hesperidin administration. Moreover, polyacrylamide gel electrophoresis analysis of serum lipoproteins revealed that the very low-density lipoprotein (VLDL)/low-density lipoprotein (LDL) ratio and LDL migration index of the high-TG type were remarkably higher than those of the other phenotypes but that their high values were significantly reduced by the administration. These results indicate that G-hesperidin preferentially lowers serum TG in hypertriglyceridemic subjects and that this effect is possibly caused by the improvement of VLDL metabolic abnormality, leading to the reduction of small dense LDL.     

Carbohydrate restriction alters lipoprotein metabolism by modifying VLDL, LDL, and HDL subfraction distribution and size in overweight men

To determine the effects of carbohydrate restriction (CR) with and without soluble fiber on lipoprotein metabolism, 29 men participated in a 12-wk weight loss intervention. Subjects were matched by age and BMI and randomly assigned to consume 3 g/d of either a soluble fiber supplement (n=14) or placebo (n=15) with a macronutrient energy distribution of approximately 10% carbohydrate, approximately 65% fat, and approximately 25% protein. Because the groups did not differ in any of the variables measured, all data were pooled and comparisons were made between baseline and 12 wk. After 12 wk, subjects had a mean weight loss of 7.5 kg (P<0.001), and abdominal fat was reduced by 20% (P<0.001). Plasma LDL cholesterol and triglycerides (TG) were significantly reduced by 8.9 and 38.6%, respectively. Similarly, apolipoproteins C-I (-13.8%), C-III (-21.2%) and E (-12.5%) were significantly lower after the intervention. In contrast plasma HDL-cholesterol concentrations were increased by 12% (P<0.05). Changes in plasma TG were positively correlated with reductions in large (r=0.615, P<0.01) and medium VLDL particles (r=0.432, P<0.05) and negatively correlated with LDL diameter (r=-0.489, P<0.01). Changes in trunk fat were positively correlated with medium VLDL (r=0.474, P<0.0) and small LDL (r=0.405, P<0.05) and negatively correlated with large HDL (r=-0.556, P<0.01). We conclude that weight loss induced by CR favorably alters the secretion and processing of plasma lipoproteins, rendering VLDL, LDL, and HDL particles associated with decreased risk for atherosclerosis and coronary heart disease.     

Different effects of zinc and copper deficiency on composition of plasma high density lipoproteins in rats

Male Sprague-Dawley rats (six per group) were fed an egg white-based diet containing 0 or 5 micrograms/g Cu with 1, 10, 100 or 1000 micrograms/g Zn. After 6 wk of feeding, the rats were killed, and the tissues were processed for trace element, lipid and lipoprotein analysis. Copper deficiency was associated with a higher concentration of plasma free cholesterol, high density lipoprotein (HDL) cholesterol and HDL apolipoproteins. Plasma total cholesterol was not significantly affected. No significant differences were noted in HDL lipid composition. However, HDL apo E and apo A-I concentrations were higher with copper deficiency. Lecithin:cholesterol acyltransferase (LCAT) was not affected in a consistent manner by copper status. Varying the amount of zinc in the diet did not produce significant changes in plasma total cholesterol, plasma free cholesterol, HDL cholesterol, or HDL apolipoprotein concentrations. However, HDL from zinc-deficient rats were enriched in free cholesterol and depleted in triglycerides. Furthermore, the concentration of HDL apo C increased as the level of dietary zinc increased.     

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)     

Lipoprotein metabolism during and after a 6-h infusion ofMCT/LCT vs LCT emulsion in man

We studied, in man, the intravascular metabolism of two lipid emulsions differing in their triglyceride (TG) fatty acid pattern. One emulsion was composed exclusively of soy bean long-chain triglycerides (LCT), the other of a mixture containing a (1:1, wt:wt) ratio of medium-chain triglycerides (MCT) and LCT (MCT/LCT). Both emulsions contained 10% TG and 1.2% of the same egg yolk phospholipid emulsifier. Six healthy volunteers received both emulsions, in random order, at a rate of 0.2 g TG/kg.h for 6 h. An interval of 2 weeks separated the tests. Although the MCT/LCT emulsion provided 39% more TG molecules than the pure LCT emulsion, plasma TG increased to similar levels, indicating a faster elimination of MCT/LCT. The rise of plasma non esterified fatty acids was greater with MCT/LCT (P < 0.001). LDL-TG enrichment was higher with MCT/LCT (P < 0.025) while net transfer of TG to HDL was similar with both emulsions. Cholesteryl ester (CE) enrichment in the 'VLDL' fraction (largely composed of emulsion particles) was markedly less during MCT/LCT than LCT infusions (P < 0.01). CE enrichment of the 'VLDL' fraction persisted up to 6 h after cessation of both lipid infusions. In conclusion, TG from MCT/LCT emulsion appear to be eliminated faster than LCT during an in vivo infusion in man. In accordance with our previous in vitro data, MCT/LCT infusion was associated with a higher transfer of TG to LDL and in a reverse manner, with a lesser acquisition of CE by emulsion particles as compared to LCT infusion.     

Indices related to apo CII and CIII serum concentrations and coronary heart disease: a case-control study

BACKGROUND: Triglycerides (TG) are carried in the circulation by diverse lipoprotein particles, which vary in their lipid and protein content, metabolism, and atherogenicity. Several indices related to apolipoproteins (apo) CII and CIII blood concentration have been proposed to reflect TG metabolism more accurately than the blood level of TG. In the present study we compared the distribution of those indices in coronary heart disease (CHD) patients and controls.. METHODS: Ninety consecutively discharged patients with CHD and 209 healthy controls were included in the analysis. Demographic, clinical, and laboratory characteristics were obtained. RESULTS: The CHD patients differed appreciably from controls in several TG-related variables. After adjusting for cardiovascular risk factors, significant associations were found between CHD and the following: TG, VLDL-C, apo CIII, apo CIII in HDL, apo CIII in VLDL + LDL, apo CII- to- TG ratio, and apo CIII ratio (CIII in HDL/CIII in VLDL + LDL). Further adjustment for HDL-C substantially attenuated the above associations, except for those regarding apo CIII in VLDL + LDL (odds ratio (OR): 1.69 per 1 SD increment, 95%CI: 1.03-2.77) and apo CIII ratio (OR: 0.40 per 1 SD increment, 95%CI: 0.15-1.00). CONCLUSION: Our results add to the growing evidence which links apo CIII concentration in VLDL + LDL to CHD. Further confirmation in prospective studies would be required before considering this measurement as a screening tool.     

Serum apolipoprotein A-I levels: relationship to lipoprotein lipid levels and selected demographic variables

Serum apolipoprotein A-I (apo A-I) and lipoprotein cholesterol and triglycerides were measured in 289 persons randomly selected from a Northern California industrial population in 1974-1976. Apo A-I and high density lipoprotein (HDL) cholesterol were strongly correlates with one another and both were inversely correlated with very low density lipoprotein (VLDL) triglycerides. The decrease in HDL-cholesterol with increasing VLDL-triglycerides was relatively much larger than the concomitant decrease in apo A-I. The relative decrease in the sum of cholesterol and triglycerides in the HDL fraction was similar to that for apo A-I, suggesting that the decreasing HDL-cholesterol:apo A-I ratio with increasing VLDL-triglycerides is due in large part to reciprocal transfer of cholesteryl esters for triglycerides between HDL and VLDL. Mean apo A-I level was 16 mg/dl higher in women not taking exogenous sex steroids than in men, 31 mg/dl higher in women taking estrogens without progestins and 10 mg/dl higher in contraceptive drug users than in other women, and 8 mg/dl higher in black than in white men. The first two of these differences were statistically significant. Apo A-I level was unrelated to age, but increased with ethanol consumption and decreased with adiposity. An inverse relationship between Apo A-I and cigarette smoking was found among women.     

Elimination of lipofundin S during the intravenous fat tolerance test in patients with low, medium, and high fasting triglyceride concentrations

The intravenous fat tolerance test with Lipofundin S (0.5 ml of 20% emulsion/kg body weight) was performed in 22 male nondiabetic patients. According to their fasting triglycerides (TG), the patients were arranged into three groups: low (less than 2.8 mmol/liter), medium (2.8-5.7 mmol/liter), and high (greater than 5.7 mmol/liter) concentrations. Fractional elimination rates of injected Lipofundin S decreased from 11.08 in low TG to 4.57%/min in high TG; they were positively correlated with fasting levels of high-density lipoprotein cholesterol but negatively with those of TG. The same pattern of correlations was observed with fractional catabolic rates of endogenous TG as measured after injection of tritium-labeled glycerol. The intravenous Lipofundin S load effected transient TG and free fatty acid elevations which were delayed in high TG. The elimination mechanisms of injected Lipofundin S and of endogenous TG are compared.     

Differential reduction of plasma cholesterol by the American Heart Association Phase 3 Diet in moderately hypercholesterolemic, premenopausal women with different body mass indexes.

The ability of a low-fat, low-cholesterol diet to improve the risk-factor profiles of moderately hypercholesterolemic, premenopausal women was evaluated. Nineteen women were fed a typical American diet for 1 mo, after which a low-fat diet consisting of 21% of total energy (en%) as fat, 59 en% carbohydrates, 19 en% protein, and 96 mg cholesterol/d (P:S 1.8) was given. After 5 months, total and low-density lipoprotein (LDL) cholesterol was decreased by 7% and 11%, respectively, and total triglycerides increased by approximately 30%. High-density-lipoprotein (HDL) cholesterol was decreased by 12% at month 2 and 5% at month 5 (P less than 0.05). Although HDL2 cholesterol decreased progressively throughout the diet period to -35% by month 5, HDL3 cholesterol, which decreased to -5% at month 1, increased to +7% by month 5. Of the plasma apolipoproteins only apo A-II was altered (+15%) by the diet. Body mass index correlated to baseline values and affected response to diet; only the leanest women had significant decreases in total, LDL, and HDL2 cholesterol in response to the low-fat diet.     

Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch

Ten hyperinsulinemic and 11 nonhyperinsulinemic men consumed for 5 wk each in a cross-over design a diet, similar to one currently consumed in the United States, with 20% of the kilocalories from either fructose or high-amylose cornstarch to determine the effects of the two diets on various blood metabolites considered to be risk factors associated with heart disease. In the hyperinsulinemic men the intake of fructose as compared with cornstarch significantly increased total triglycerides and their lipoprotein distribution; total and very-low-density lipoprotein cholesterol; apoproteins B-100, C-II, C-III; and uric acid. In the nonhyperinsulinemic men total triglycerides, total and low-density lipoprotein cholesterol and uric acid were significantly greater after the consumption of fructose than after cornstarch. The results indicate that in a diet high in saturated fatty acids and cholesterol, fructose increases the levels of risk factors associated with heart disease, especially in hyperinsulinemic men.