Cholesterol Articles and Abstracts

For medical practitioners and the general public - Cholesterol Journal Article Catalog.

Cholesterol Journal Articles



Record 5701 to 5720
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Efficacy of dietary aloe vera supplementation on hepatic cholesterol and oxidative status in aged rats
Lim, B. O., N. S. Seong, et al. (2003), J Nutr Sci Vitaminol (Tokyo) 49(4): 292-6.
Abstract: In the current study, we show the anti-oxidative and hypocholesterol effects of aloe vera in the liver. Male specific pathogen-free (SPF) Fischer 344 rats were randomly assigned to one of four groups: Group A (control) was fed test chow without aloe supplementation; Group B was fed a diet containing a 1% (per weight basis) freeze-dried aloe filet; Group C was fed a diet containing a 1% (per weight basis) charcoal-processed, freeze-dried aloe filet; and Group D was fed a diet containing a charcoal-processed freeze-dried, whole leaf aloe (0.02% per weight basis) in the drinking water. Our results show that a life-long intake of aloe had superior anti-oxidative action against lipid peroxidation in vivo, as indicated by reduced levels of hepatic phosphatidylcholine hydroperoxide. Additional anti-oxidative action was evidenced by enhanced superoxide dismutase (SOD) and catalase activity in groups B and C. Furthermore, our study revealed that hepatic cholesterol significantly increased in the control group during aging in contrast to the aloe-supplemented groups, which showed approximately 30% lower cholesterol levels, thereby an effective hypocholesteremic efficacy. In this report, we suggest that life-long dietary aloe supplementation suppresses free radical-induced oxidative damage and age-related increases in hepatic cholesterol.

Efficacy of dietary fiber in lowering serum cholesterol
Garg, A. (1994), Am J Med 97(6): 501-3.

Efficacy of fish oil supplementation for treatment of moderate elevation of serum cholesterol
Valdini, A. F., M. A. Glenn, et al. (1990), J Fam Pract 30(1): 55-9.
Abstract: A study was performed to determine the efficacy and feasibility of using fish oil capsules for treatment of moderate hypercholesterolemia. Thirty-three subjects, randomized to fish or olive oil, took two 1-g capsules with each meal for 12 weeks. Each subject crossed over to the alternate treatment at 12 weeks. Patients maintained usual levels of exercise and diet for 24 weeks. Eight subjects dropped out. For the group starting fish oil (n = 13), the average baseline cholesterol level was 6.336 mmol/L (245.0 mg/dL) and was 6.341 mmol/L (245.2 mg/dL) after 12 weeks. High-density lipoprotein cholesterol (HDL-C) and calculated low-density lipoprotein cholesterol (LDL-C) baseline levels were 1.459 mmol/L (56.4 mg/dL) and 4.332 mmol/L (167.5 mg/dL); 1.474 mmol/L (57.0 mg/dL) and 4.479 mmol/L (173.2 mg/dL), respectively, after fish oil supplementation. In the group that began with olive oil (n = 12), baseline total cholesterol level was 6.274 mmol/L (242.6 mg/dL); HDL-C and calculated LDL-C baseline levels were 1.386 mmol/L (53.6 mg/dL) and 3.988 mmol/L (154.2 mg/dL). When mean baseline levels were compared with post-fish-oil values for the entire population, no significant change in total cholesterol or LDL-HDL ratio was obtained. Triglyceride responses to fish oil were variable. Values after olive oil treatment were neither significantly different from baseline nor different from fish oil. It was concluded that fish oil in manufacturer's recommended dosage does not appear to lower moderately elevated cholesterol levels.

Efficacy of garlic supplementation in lowering serum cholesterol levels
Spigelski, D. and P. J. Jones (2001), Nutr Rev 59(7): 236-41.
Abstract: Previous studies using garlic have found alterations on a number of cardiovascular disease (CVD) risk factors including blood pressure, plasma viscosity, platelet activity, and serum lipid levels. The latest clinical research suggests that consumption of garlic powder does not play a significant role in lowering plasma lipid levels when in conjunction with a low-fat, low-cholesterol diet. Additional well-controlled, long-term studies that explore dosage and preparation type are necessary to confirm the efficacy of garlic in lowering cholesterol levels and to fully understand garlic's potential role in CVD.

Efficacy of psyllium in reducing serum cholesterol levels in hypercholesterolemic patients on high- or low-fat diets
Sprecher, D. L., B. V. Harris, et al. (1993), Ann Intern Med 119(7 Pt 1): 545-54.
Abstract: OBJECTIVES: To determine the efficacy of psyllium in reducing serum cholesterol levels in patients on high- or low-fat diets. DESIGN: Double-blind, placebo-controlled, 16-week parallel trial. The study included an 8-week baseline period and an 8-week treatment period. PATIENTS: Healthy men and women, 21 to 70 years old, with primary hypercholesterolemia (total serum cholesterol > or = 5.7 mmol/L 220 mg/dL). Thirty-seven participants followed a high-fat diet and 81 participants followed a low-fat diet. INTERVENTION: Participants were randomly assigned to either psyllium, 5.1 g twice a day, or placebo. MEASUREMENTS: Fasting lipid and apolipoprotein concentrations, including direct low-density lipoprotein (LDL) cholesterol quantification; nutritional analyses of 4 days of 7-day food records to monitor dietary compliance; and physical examinations, clinical chemistry and hematologic studies, and urinalysis to assess treatment safety. MAIN RESULTS: Psyllium recipients in both the high- and low-fat diet groups showed small but significant decreases (P < 0.05) in total cholesterol and low-density lipoprotein (LDL) cholesterol levels. Total cholesterol and LDL cholesterol levels decreased 5.8% and 7.2%, respectively, in psyllium recipients on high-fat diets and 4.2% and 6.4%, respectively, in psyllium recipients on low-fat diets. No significant difference was seen in LDL cholesterol response when psyllium recipients on low- and high-fat diets were compared (P > 0.2). No significant reductions in lipid levels were observed in placebo recipients. Based on the National Cholesterol Education Program LDL cholesterol classification system, 39% of the psyllium recipients improved in LDL cholesterol classification (P < 0.0001) compared with 20.3% of placebo recipients (P > 0.2). CONCLUSIONS: Psyllium produces a modest but significant improvement in total cholesterol and LDL cholesterol levels in persons on either low-fat or high-fat diets. Psyllium, when added to a prescribed low-fat diet, may obviate the need for typical lipid-lowering medications or may prove to be a valuable adjunct to other treatments in patients with moderately elevated LDL cholesterol levels.

Efficacy of raising high-density lipoprotein cholesterol for prevention of coronary heart disease
Teramoto, T. (2002), Curr Atheroscler Rep 4(5): 327-8.

Efficacy of simvastatin for lowering cholesterol in non-insulin dependent diabetic patients with hypercholesterolemia
Daubresse, J. C., R. Machowski, et al. (1994), Acta Clin Belg 49(2): 68-75.
Abstract: Patients with non-insulin-dependent diabetes mellitus (NIDDM) are at high risk of cardiovascular disease for many reasons and especially due to the fact that dyslipidemias are more frequent in this group of patients. Fibrate derivatives are the drugs of choice when hypertriglyceridemia is the main lipid anomaly. When hypercholesterolemia is predominant, the use of resins and nicotinic acid has been advocated but these drugs are poorly tolerated on a long-term basis. We assessed the effect of simvastatin, a recent HMG-CoA reductase inhibitor in 12 NIDDM patients with hypercholesterolemia. After 4 weeks of placebo, which did not significantly modify the lipid values, patients were given simvastatin at increasing dosages (from 10 to a maximum of 40 mg daily) during 24 weeks. Compliance and clinical tolerance were excellent. There was no major biological side effect, but a significant deterioration of glucose control was noted at the end of the study. Simvastatin reduced total cholesterol by 28%, LDL-cholesterol by 36% and apo B by 31%. Concomitantly, there was an increase of HDL-cholesterol by 15%. This improvement of lipid profile persisted during the 24 weeks of treatment. Comparing the patients with pure hypercholesterolemia to those presenting combined hyperlipidemia, it was evident that the hypolipidemic effect was more marked in the diabetic subjects with combined hyperlipidemia.

Efficiency of intestinal cholesterol absorption in humans is not related to apoE phenotype
Von Bergmann, K., D. Lutjohann, et al. (2003), J Lipid Res 44(1): 193-7.
Abstract: The present study investigated the role of apolipoprotein E (apoE) phenotype on intestinal cholesterol absorption and cholesterol synthesis. Studies were carried out in eight subjects homozygous for the apoE4 and 12 subjects homozygous for the E2 allele (six normocholesterolemic volunteers and six patients with type III hyperlipoproteinemia). Cholesterol absorption did not differ between the three groups of subjects and averaged 38 +/- 2% (mean +/- SEM) in normolipemic E2/2, 37 +/- 4% in type III hyperlipemic E2/2, and 41 +/- 3% in E4/4 subjects, respectively. Dietary intake of fat and cholesterol had no influence on cholesterol absorption efficiency. A positive correlation between efficiency of cholesterol absorption and the ratio of campesterol to cholesterol in plasma, an indirect marker for cholesterol absorption, was observed after combining the results of the three groups (r = 0.504; P < 0.02). Bile acid and total cholesterol synthesis were also not affected by the different apoE alleles, but the well-known relationship between body weight and cholesterol synthesis was noticed (r = 0.574; P < 0.01). Thus, the present study provides evidence that the efficiency of intestinal absorption and synthesis of cholesterol in humans are not related to the apoE phenotype.

Efficient coexpression and secretion of anti-atherogenic human apolipoprotein AI and lecithin-cholesterol acyltransferase by cultured muscle cells using adeno-associated virus plasmid vectors
Fan, L., J. Drew, et al. (1998), Gene Ther 5(10): 1434-40.
Abstract: Plasma apolipoprotein AI (apoAI) and lecithin-cholesterol acyltransferase (LCAT) play important roles in reverse cholesterol transport, promoting the removal of excess cholesterol from peripheral cells and reducing formation of atherosclerotic lesions. Gene augmentation of either apoAI or LCAT, or both, are thus attractive targets for prevention or treatment of atherosclerosis. With the eventual aim of safe and efficient gene delivery to skeletal muscle, our chosen secretory platform for systemic delivery of anti-atherogenic proteins, we have constructed conventional and AAV-based plasmid vectors containing human apoAI or LCAT cDNAs; their efficacy was tested by lipoplex transfection of mouse C2C12 muscle cells or human 293 cells. The secretion of apoAI or LCAT by transduced cultures was two- to five-fold higher using AAV-based plasmid vectors than conventional plasmid vectors. Additionally, cells transfected with a bicistronic AAV-based vector containing an internal ribosome entry site (IRES) efficiently expressed both apoAI and LCAT simultaneously. Furthermore, AAV-based vector sequences were retained by host cells, whereas those of conventional plasmid vectors were lost. These studies indicate that ectopic overexpression of apoAI and LCAT in muscle tissue using AAV-based plasmid vectors might provide a feasible anti-atherogenic strategy in vivo.

Efflux of cellular cholesterol and phospholipid to apolipoprotein A-I mutants
Sviridov, D., L. E. Pyle, et al. (1996), J Biol Chem 271(52): 33277-83.
Abstract: Human plasma apolipoprotein A-I (apoA-I) and recombinant full-length proapoA-I (apoA-I-(-6-243)) as well as four truncated forms of proapoA-I were used as acceptors to study cholesterol and phospholipid efflux from HepG2 cells. Efflux of both cholesterol and phospholipid to the lipid-free plasma apoA-I was twice that of apoA-I-(-6-243). When apoA-I was incorporated into reconstituted high density lipoprotein, cholesterol efflux increased, phospholipid efflux decreased and the difference between plasma apoA-I and apoA-I-(-6-243) disappeared. Truncation of recombinant apoA-I to residues 222 (apoA-I-(-6-222)) and 210 (apoA-I-(-6-210)) resulted in a 70-95% decrease in their ability to promote the efflux of both intracellular and plasma membrane cholesterol. Further truncation to residues 150 (apoA-I-(-6-150)) and 135 (apoA-I-(-6-135)) fully restored the ability of apoA-I to promote cholesterol efflux. Phospholipid efflux closely paralleled the efflux of cholesterol. Interaction of 125I-labeled apoA-I with the cells was similar for apoA-I-(-6-243), apoA-I-(-6-222), and apoA-I-(-6-210), but slightly higher for apoA-I-(-6-150) and apoA-I-(-6-135). When complexed with phospholipid, all forms except apoA-I-(-6-210) formed discoidal reconstituted high density lipoprotein particles. When the same amounts of free or lipid-associated apoA-I were compared, association of apoA-I with phospholipid increased cholesterol efflux and decreased phospholipid efflux, and the difference in the ability of different mutants to promote cholesterol and phospholipid efflux disappeared. We conclude that the capacity of lipid-free apoA-I to promote cholesterol efflux is related to its ability to mobilize cellular phospholipid, which apparently involves a region around residues 222-243. A second lipid-binding region is exposed when the carboxyl-terminal half of apoA-I is absent.

Efflux of cellular cholesterol and phospholipid to lipid-free apolipoproteins and class A amphipathic peptides
Yancey, P. G., J. K. Bielicki, et al. (1995), Biochemistry 34(24): 7955-65.
Abstract: The mechanism(s) by which lipid-free apolipoprotein (apo) AI is able to stimulate efflux of cholesterol and phospholipid from cells in cultures has (have) been examined. This process was found to be enhanced when macrophages were enriched with cholesterol. There were 12- and 4-fold increases in cholesterol and phospholipid efflux, respectively, from cholesterol-enriched mouse macrophages when compared to cells not loaded with cholesterol. This enhancement in cholesterol efflux to lipid-free apo AI from macrophages enriched with cholesterol was found to be controlled by the level of free cholesterol in the cells. When cholesterol-enriched mouse macrophages were exposed to lipid-free apo AI at 20 micrograms/mL (706 nM), there was significant efflux of 14Ccholesterol and 3Hphospholipid (20% +/- 0.5%/24 h and 6% +/- 0.3%/24 h, respectively). In comparison, HDL at equivalent protein concentrations only stimulated 11% and 4% efflux of cholesterol and phospholipid, respectively. Synthetic peptides containing amphipathic helical segments that mimic those present in apo AI were used to examine the structural features of the apoprotein which stimulate lipid efflux. Peptides containing only one (18A) or two (37pA) amphipathic helical segments stimulated as much cholesterol efflux from both mouse macrophages and L-cells as apo AI. The order of efficiency, as assessed by the mass concentration at which half-maximal efflux was reached (EC50), was apo AI > 37pA > 18A, indicating that acceptor efficiency was dependent on the number of amphipathic helical segments per molecule. When the helical content of 18A was increased by neutralizing the charges at the ends of the peptide (Ac-18A-NH2), there was a substantial increase in the efficiency for cholesterol efflux (EC50 18A = 17 micrograms/mL vs Ac-18A-NH2 = 6 micrograms/mL). In contrast, when the amphipathicity of the helix in 18A was decreased by scrambling the amino acid sequence, thereby reducing its lipid affinity, cholesterol and phospholipid efflux were not stimulated. The efficiency with which the peptides stimulated cholesterol efflux was in order of their lipid affinity (37pA > Ac-18A-NH2 > 18A), and this order was similar for phospholipid efflux. The time course of lipid release from mouse macrophages and L-cells indicated that phospholipid appeared in the extracellular medium before cholesterol. These results suggest that the apo AI or peptides first interacted with the cell to form protein/phospholipid complexes, that could then accept cholesterol.

Efflux of cholesterol from cholesterol loaded macrophages by incubation with synthetic HDL-particles
Westman, J., C. Roobol, et al. (1993), Scand J Clin Lab Invest 53(8): 773-82.
Abstract: Cells from the mouse monocyte/macrophage cell line J774A.1 were incubated with acetylated human low density lipoprotein for 2 days, resulting in an intracellular accumulation of mainly cholesteryl esters. These in vitro foam cell models were used to study the capability of synthetic HDL-particles to promote efflux of cholesterol. The synthetic HDL-particles were prepared from recombinant human pro-apolipoprotein A-I or human apolipoprotein A-I and phosphatidylcholine. Both types of reconstituted complexes were found to have a discoidal structure. A 24 h incubation of lipid loaded J774A.1 cells with these two types of discoidal complexes resulted in an equivalent and marked egress of cholesterol. The effect was the same whether the origin of phosphatidylcholine was egg yolk or soybean.

Efflux of cholesterol from different cellular pools
Haynes, M. P., M. C. Phillips, et al. (2000), Biochemistry 39(15): 4508-17.
Abstract: Free cholesterol is very efficiently removed from cells by 2-hydroxypropyl-beta-cyclodextrins. The efflux of cholesterol occurs from two distinct kinetic pools: the half-times (t(1/2)) for the two pools in CHO-K1 cells are 15 +/- 5 s and 21 +/- 6 min and they represent 25% +/- 5% and 75% +/- 5% of the readily exchangeable cell cholesterol, respectively. In this study we have determined that the fast pool and the majority of the slow kinetic pool for cholesterol efflux are apparently present in the plasma membrane. Numerous agents that inhibit intracellular cholesterol trafficking are unable to affect either the size or the t(1/2) for efflux of either kinetic pool. In contrast, treatment of the cells with N-ethylmaleimide (NEM), exogenous lipases such as sphingomyelinase and phospholipase C, calcium ionophore A23187, or heat resulted in the dramatic increase in the size of the fast kinetic pool of cholesterol. These changes in the kinetics of cholesterol efflux are not specific to the nature of the extracellular acceptor indicating that they are a consequence of changes in the cell plasma membrane. The above treatments disrupt the normal organization of the lipids in the plasma membrane via either hydrolysis or randomization. The phosphatidylcholine and sphingomyelin present in the plasma membrane are critical for maintaining the two kinetic pools of cholesterol; any alteration in the amount or the location of these phospholipids results in an enhancement of efflux by redistributing cholesterol into the fast kinetic pool.

Efflux of intracellular versus plasma membrane cholesterol in HepG2 cells: different availability and regulation by apolipoprotein A-I
Sviridov, D. and N. Fidge (1995), J Lipid Res 36(9): 1887-96.
Abstract: We have compared the efflux of cholesterol from different cellular pools of human hepatoma cells HepG2 using intact cells or isolated membrane fractions. To label different pools, cells were incubated with either unesterified 14Ccholesterol that had been incorporated into high density lipoproteins (14CFC-HDL), low density lipoproteins (14CFC-LDL), or phosphatidylcholine liposomes (14CFC-PC), or with 14Cacetate. Cell fractionation revealed that labeling of cells with 14CFC-PC resulted in the incorporation of 14Ccholesterol almost exclusively into the plasma membrane (PM), while incubation with 14CFC-HDL resulted in the majority of 14Ccholesterol incorporation into the PM, but with a smaller component associated with lysosomes. Labeling with 14CFC-LDL or 14Cacetate led to an accumulation of 14Ccholesterol predominantly in lysosomes or the endoplasmic reticulum (ER), respectively. When the kinetics of 14Ccholesterol efflux was analyzed after pulse-labeling of different cellular pools, half-times of cholesterol efflux from lysosomes and ER were significantly longer than that from PM. In another set of experiments, when both labeling and efflux times varied, efflux of 14Ccholesterol from the PM to human serum after 1.5 h pulse and chase incubations was double that from lysosomes and 8-fold that from ER. Extension of the incubation times from 1.5 to 3 h diminished the difference in cholesterol efflux from different membranes. Further incubation to 6 h almost abolished the different responses. Cell-free preparations of membranes, obtained from cells labeled with 14Ccholesterol, showed no differences in cholesterol efflux. No differences in the distribution of 14Ccholesterol released into serum among lipoprotein subfractions was observed. Pretreatment of the serum with Fab fragments of polyclonal rabbit anti-human apolipoprotein A-I antibodies reduced its ability to promote efflux of cholesterol from the ER by 77%, but had no effect on cholesterol efflux from the PM. Fab fragments of non-immune IgG had no effect on the efflux of both ER and PM cholesterol. We conclude that the availability of cellular cholesterol for efflux from HepG2 cells is strongly influenced by its subcellular location, and is regulated by apolipoprotein A-I.

Efflux of lipid from fibroblasts to apolipoproteins: dependence on elevated levels of cellular unesterified cholesterol
Bielicki, J. K., W. J. Johnson, et al. (1992), J Lipid Res 33(11): 1699-709.
Abstract: Earlier work from this laboratory showed that enrichment of cells with free cholesterol enhanced the efflux of phospholipid to lipoprotein acceptors, suggesting that cellular phospholipid may contribute to high density lipoprotein (HDL) structure and the removal of sterol from cells. To test this hypothesis, we examined the efflux of 3Hcholesterol (FC) and 32Pphospholipid (PL) from control and cholesterol-enriched fibroblasts to delipidated apolipoproteins. The percentages of 3Hcholesterol and 32Pphospholipid released from control cells to human apolipoprotein A-I were 2.2 +/- 0.5%/24 h and 0.8 +/- 0.1%/24 h, respectively. When the cellular cholesterol content was doubled, efflux of both lipids increased substantially (3HFC efflux = 14.6 +/- 3.6%/24 h and 32PPL efflux = 4.1 +/- 0.3%/24 h). Phosphatidylcholine accounted for 70% of the radiolabeled phospholipid released from cholesterol-enriched cells. The cholesterol to phospholipid molar ratio of the lipid released from cholesterol-enriched cells was approximately 1. This ratio remained constant throughout an incubation time of 3 to 48 h, suggesting that there was a coordinate release of both lipids. The concentrations of apoA-I, A-II, A-IV, E, and Cs that promoted half-maximal efflux of phospholipid from cholesterol-enriched fibroblasts were 53, 30, 68, 137, and 594 nM, respectively. With apoA-I and A-IV, these values for half-maximal efflux of phospholipid were identical to the concentrations that resulted in half-maximal efflux of cholesterol. Agarose gel electrophoresis of medium containing apoA-I that had been incubated with cholesterol-enriched fibroblasts revealed a particle with alpha to pre-beta mobility. We conclude that the cholesterol content of cellular membranes is an important determinant in the ability of apolipoproteins to promote lipid removal from cells. We speculate that apolipoproteins access cholesterol-phosphatidylcholine domains within the plasma membrane of cholesterol-enriched cells, whereupon HDL is generated in the extracellular compartment. The release of cellular lipid to apolipoproteins may serve as a protective mechanism against the potentially damaging effects of excess membrane cholesterol.

Efflux of newly synthesized cholesterol and biosynthetic sterol intermediates from cells. Dependence on acceptor type and on enrichment of cells with cholesterol
Johnson, W. J., R. T. Fischer, et al. (1995), J Biol Chem 270(42): 25037-46.
Abstract: Previous studies suggest that during sterol synthesis in cells, cholesterol and precusor sterols are transported to the plasma membrane and that this transport is stimulated by the binding of high density lipoprotein (HDL) to its putative cell surface receptor, leading to enhanced sterol efflux. Little is known about the identities of synthesized sterols subject to efflux or whether efflux of cholesterol and precursor sterols are stimulated equally by HDL. To address these issues, cells were incubated with 3Hacetate or 3Hmevalonate and sterol acceptors, and then the labeled sterols in cells and efflux media were analyzed by high pressure liquid chromatography methods that resolved cholesterol and precursor sterols. In non-hepatic cells (Chinese hamster ovary (CHO), fibroblasts, and smooth muscle), cholesterol and multiple precursor sterols accumulated. In CHO cells, the major products were cholesterol and desmosterol, which together constituted 50% of labeled nonsaponifiable lipids. When media contained human HDL3 (1 mg of protein/ml), the molar efflux of synthesized desmosterol was four times that of cholesterol, and the 8-h efflux of these sterols, each normalized to its own production, averaged 48 and 16%, respectively. When media contained egg phosphatidylcholine vesicles (1 mg/ml), the efflux of these sterols averaged 18 and 2.4%, respectively. Thus, with both acceptors, desmosterol was the major synthesized sterol released from cells, and its efflux was substantially greater than that of synthesized cholesterol. High relative efflux of desmosterol (or a desmosterol-like sterol) occurred in all cell types and in both cholesterol-enriched and unenriched cells. These results demonstrated qualitatively similar efflux of synthesized sterols in the presence of HDL3 and phospholipid vesicles, arguing against an absolute requirement for acceptors that interact with the HDL receptor. To probe for possible quantitative differences in the capabilities of these two acceptors, the ratios of (efflux to HDL3)/(efflux to phosphatidylcholine vesicles) were calculated for synthesized cholesterol and desmosterol, plasma membrane cholesterol, and lysosomal cholesterol. In comparison to plasma membrane cholesterol, there was little or no HDL selectivity for lysosomal cholesterol or synthesized desmosterol, whereas there was a 2-3-fold selectivity for synthesized cholesterol, suggesting that the ability of HDL to enhance the efflux of synthesized sterols is a modest quantitative effect and confined to cholesterol.

Efflux of phospholipid from fibroblasts with normal and elevated levels of cholesterol
Bielicki, J. K., W. J. Johnson, et al. (1991), Biochim Biophys Acta 1085(1): 7-14.
Abstract: To address the hypothesis that phospholipid efflux from cells contributes to lipoprotein structure, we have examined the efflux of biosynthetically labeled 32Pphospholipid from cells to lipoproteins. With normal human skin fibroblasts in monolayer culture, high density lipoprotein (HDL3) promoted the efflux of phospholipid in a concentration-dependent manner. As analyzed by TLC, the major phospholipids released from fibroblasts were phosphatidylcholine, sphingomyelin, lysophosphatidylcholine and phosphatidylethanolamine. At identical concentrations, HDL3 and dimethylsuberimidate treated-HDL3 promoted similar efflux, suggesting that efflux did not depend on specific binding of HDL3 to the cell surface. When the content of cholesterol in fibroblasts was doubled by pre-incubation with LDL and cholesterol-rich liposomes, the fractional efflux of phospholipid to HDL3 and other acceptors was stimulated about 2-fold. Most of this stimulation was due to enhanced release of phosphatidylcholine. Similar effects of enrichment were found with Fu5AH rat hepatoma cells, but not with J774 mouse macrophages. The results support the hypothesis that the efflux of phospholipid from cells contributes to the phospholipid content of HDL. This may enhance the ability of HDL to remove cholesterol from cells, the initial step in reverse cholesterol transport.

Effort angina in a middle-aged woman with abnormally high levels of serum high-density lipoprotein cholesterol: a case of cholesteryl-ester transfer protein deficiency
Nagano, M., M. Nakamura, et al. (2005), Circ J 69(5): 609-12.
Abstract: A 54-year-old female was admitted to hospital complaining of oppressive anterior chest pain during exercise. Treadmill exercise ECG testing showed significant ischemic ECG changes, and electron-beam computed tomography demonstrated patchy calcifications in the coronary artery. Coronary angiography revealed a significant stenotic lesion of the right coronary artery. On routine investigations, no classical coronary risk factors were found, although a very high concentration (209 mg/dl) of high-density lipoprotein cholesterol (HDL-C) was detected. The serum concentration of cholesteryl-ester transfer protein (CETP), which plays a central role in the reverse cholesterol transport system, was measured and found to be less than the measurable minimum. The patient showed one of the typical genetic CETP mutations (intone 14 splicing defect), and her lipid profile was improved by administration of probucol for 3 months. A very high concentration of HDL-C with a defect of CETP activity may be a specific biochemical indicator pointing to an increased risk of premature coronary artery disease, and the lipid profile can be improved by use of lipid-lowering drugs.

Egg consumption and high-density-lipoprotein cholesterol
Schnohr, P., O. O. Thomsen, et al. (1994), J Intern Med 235(3): 249-51.
Abstract: OBJECTIVES. To examine if increased egg consumption raises serum high-density-lipoprotein (HDL) cholesterol in healthy individuals. DESIGN. A cross-over study. SETTING. A private clinic for preventive health examinations in Copenhagen. SUBJECTS. Twenty-four healthy adults, 12 men and 12 women, aged 23-52 (median 40) years. INTERVENTIONS. After a 1-week control period each person added two boiled eggs to the usual daily diet for 6 weeks. All persons were instructed not to change the lifestyle in other ways during the whole study period. MAIN OUTCOME MEASURES. Serum HDL cholesterol, total cholesterol and triglycerides were measured before, during and after 6 weeks of extra egg consumption. The corresponding serum low-density-lipoprotein (LDL) cholesterol was calculated from the Friedewald formula. RESULTS. After 6 weeks of extra egg consumption serum HDL cholesterol increased by 10% (P < 0.05) and total cholesterol increased 4% (P < 0.05), whereas the ratio total cholesterol/HDL cholesterol did not change significantly. Serum triglycerides and LDL cholesterol were also unchanged. CONCLUSIONS. A moderate egg intake should not be rigorously restricted in healthy individuals.

Egg consumption and serum cholesterol
Hegsted, D. M. (1993), Am J Clin Nutr 57(1): 87-9.


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