Cholesterol Journal Articles

Record 6841 to 6860

High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport
Assmann, G., H. Schulte, et al. (1996), Atherosclerosis 124 Suppl: S11-20.
Abstract: The incidence of coronary heart disease (CHD) was assessed via the Prospective Cardiovascular Munster (PROCAM) study in 19,698 volunteer subjects aged between 16 and 65 years. An adequate incidence of atherosclerotic CHD was only found in male subjects greater than 40 years of age. The analysis and subsequent 6 year follow-up period was, therefore, confined to 4559 male participants aged 40-64 years. In the follow-up period, 186 study participants developed atherosclerotic CHD (134 definite non-fatal myocardial infarctions (MIs) and 52 definite atherosclerotic CHD deaths including 21 sudden cardiac deaths and 31 fatal MIs). Univariate analysis revealed a significant association between the incidence of atherosclerotic CHD and high-density lipoprotein cholesterol (P < 0.001), which remained after adjustment for other risk factors.

High-density lipoprotein cholesterol as a therapeutic target to reduce cardiovascular events
Fonarow, G. C. and K. E. Watson (2004), Am Heart J 147(6): 939-41.

High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: assessing the data from Framingham to the Veterans Affairs High--Density Lipoprotein Intervention Trial
Boden, W. E. (2000), Am J Cardiol 86(12A): 19L-22L.
Abstract: The Framingham Heart Study found that high-density lipoprotein cholesterol (HDL-C) was the most potent lipid predictor of coronary artery disease risk in men and women >49 years of age. The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), in which subjects were randomized to treatment with lovastatin or placebo, also reported a striking benefit of treatment, particularly in patients with HDL-C < or =35 mg/dL at baseline. Treatment with lovastatin was associated with a remarkable 45% reduction in events for this group. The Veterans Affairs HDL Intervention Trial (VA-HIT) randomized subjects to gemfibrozil or placebo. A high proportion of enrolled subjects with low HDL-C also had characteristics of the dysmetabolic syndrome. HDL-C likewise increased by 6% on treatment, total cholesterol was reduced by 4% and triglycerides by 31%. There was no change in low-density lipoprotein cholesterol (LDL-C) levels. These changes in lipid were associated with a cumulative 22% reduction in the trial primary endpoint of all-cause mortality and nonfatal myocardial infarction (MI). Additionally, significant reductions in secondary endpoints including death from coronary artery disease, nonfatal MI, stroke, transient ischemic attack, and carotid endarterectomy were associated with the increase in HDL-C. In VA-HIT, for every 1% increase in HDL-C, there was a 3% reduction in death or MI, a therapeutic benefit that eclipses the benefit associated with LDL-C reduction.

High-density lipoprotein cholesterol as an indicator of liver function and prognosis in noncholestatic cirrhotics
Habib, A., A. A. Mihas, et al. (2005), Clin Gastroenterol Hepatol 3(3): 286-91.
Abstract: BACKGROUND AND AIMS: The liver plays a central role in production and degradation of lipoproteins. Declining lipoprotein cholesterol may reflect deteriorating liver function. METHODS: We reviewed the records of 248 veterans with noncholestatic cirrhosis followed in our clinics or referred for liver transplantation between January 1, 1997 and October 31, 2002 (analysis period) and confirmed our findings prospectively in 165 noncholestatic cirrhotic veterans newly referred for liver transplantation between November 1, 2002 and May 1, 2004 (validation period). RESULTS: In the analysis group, albumin, bilirubin, INR, and Model for End-Stage Liver Disease (MELD) score correlated strongly with high-density lipoprotein (HDL) cholesterol, weakly but significantly with total cholesterol and very-low-density lipoprotein cholesterol (VLDL), and poorly with low-density lipoprotein cholesterol (LDL). Transplant-free mortality at 90, 180, and 365 days was 17/201 (8.5%), 19/173 (11.0%), and 38/119 (31.9%), respectively. Death at all 3 time points was associated with significantly lower initial levels of HDL, VLDL, and total cholesterol, but not LDL cholesterol. Of the lipoproteins, HDL was the best predictor of survival at 180 and 365 days (concordance statistics.86+/-.05 and.78+/-.05, respectively). By multivariate logistic regression, HDL cholesterol and MELD score were independent predictors of survival at 6 and 12 months. By Cox regression, HDL cholesterol below 30 mg/dL was associated with 3.4-fold increase in the hazard ratio for cirrhotic death. In the validation period, HDL cholesterol was confirmed to be significantly associated with death or transplantation at 6 or 12 months. CONCLUSIONS: HDL cholesterol in noncholestatic cirrhotic patients is a liver function test and an indicator of prognosis.

High-density lipoprotein cholesterol concentrations and postheparin hepatic and lipoprotein lipases in obesity: relationships with plasma insulin levels
Cominacini, L., U. Garbin, et al. (1993), Ann Nutr Metab 37(4): 175-84.
Abstract: The concentration of high-density lipoprotein (HDL) cholesterol in patients with severe obesity is generally subnormal. The exact mechanism linking obesity with reduced levels of HDL cholesterol remains unclear. In this study we evaluated the postheparin plasma lipolytic enzymes lipoprotein lipoprotein lipase (LPL) and hepatic lipase (HL) in a group of 24 obese women compared with controls and analyzed the interrelationships between insulin, postheparin lipolytic enzymes and HDL subfractions. Total HDL cholesterol was significantly lower in the obese subjects than in the controls, and the difference was mainly due to HDL2 cholesterol concentrations. Mean fasting glucose, insulin and the summated means of glucose (sigma glucose) after the oral glucose tolerance test (OGTT) were not significantly different in the two groups. The summated means of insulin (sigma IRI) after the OGTT were significantly higher in the obese women than in the controls. LPL, HL and the HL-to-LPL ratio were significantly higher in the obese women than in the controls. HL and LPL correlated positively with sigma glucose, sigma IRI and body mass index (BMI) and negatively with plasma triglycerides. Partial correlation analysis demonstrated that, when exposed to similar sigma IRI values, HL and LPL were no longer correlated with sigma glucose, plasma triglycerides and BMI. HDL2 cholesterol levels were negatively correlated with HL, posthepatic plasma lipolytic activity, sigma glucose, plasma triglycerides and BMI. HDL2 cholesterol concentrations were directly correlated with LPL. Partial correlation analysis showed that when exposed to similar HL and LPL values, HDL2 cholesterol values were no longer correlated with sigma glucose, sigma IRI, plasma triglycerides and BMI. Therefore, our results demonstrate that the low HDL2 cholesterol levels found in obese women may be related to the high levels of HL and to the high HL-to-LPL ratio which in turn could be determined by the peripheral insulin resistance.

High-density lipoprotein cholesterol elevation with gemfibrozil: effects of baseline level and modifying factors
Manttari, M., L. Tenkanen, et al. (1993), Clin Pharmacol Ther 54(4): 437-47.
Abstract: The effects of baseline level and modifying factors on gemfibrozil-induced high-density lipoprotein (HDL) cholesterol elevation were studied in 1028 participants with good compliance in the Helsinki Heart Study. The absolute (mmol/L) increment in HDL cholesterol was independent of baseline when the change in the placebo group (regression toward the mean) was considered. In contrast, absolute reductions in low-density lipoprotein (LDL) cholesterol and triglycerides correlated with their baselines, relative percentage changes being constant. Statistically, this could indicate differences in the mode of action of gemfibrozil: an independent and additive effect on HDL cholesterol and a multiplicative effect on LDL cholesterol and triglycerides. These differences may have a physiologic background because the main effect of gemfibrozil is in the stable HDL3 subfraction, rather than in the variable HDL2. Only 13% of the variation in gemfibrozil-induced HDL cholesterol changes were explained by modifying factors. The basic assumptions in the uses of absolute or relative changes as a measure of treatment effect are discussed.

High-density lipoprotein cholesterol in patients with psoriatic arthritis
Skoczynska, A. H., B. Turczyn, et al. (2003), J Eur Acad Dermatol Venereol 17(3): 362-3.

High-density lipoprotein cholesterol in the cardiovascular equation: does the "good" still count?
Alsheikh-Ali, A. A., J. T. Kuvin, et al. (2005), Atherosclerosis 180(2): 217-23.
Abstract: This article will discuss our current understanding of the role of HDL-C in the statin era, focusing on the question as to whether HDL-C still "counts" when determining cardiovascular risk. Epidemiologic evidence consistently demonstrates that low HDL-C is a strong and independent risk factor for CHD. The epidemiologic evidence is complimented by clinical data showing that interventions that raise HDL-C are associated with reductions in CHD risk, as well as by a growing body of experimental data demonstrating biologically plausible mechanisms that may underlie the observed clinical findings. Analyses of large statin trials also indicate that the significant and independent relationship between HDL-C and CHD risk persists despite the therapeutic effects of statins, and that HDL-C levels in statin-treated patients, both at baseline and in response to statin therapy, are relevant. Early studies on novel HDL targeting therapies are promising, but their long term safety profile and impact on clinical outcomes is yet to be determined in larger studies. Recent guidelines emphasize low HDL-C as an independent risk factor for cardiovascular disease, specifically identify HDL-C as a target for intervention, and encourage the use of HDL-C raising interventions in high-risk patients with low HDL-C levels.

High-density lipoprotein cholesterol is low in HIV-infected patients with lipodystrophic fat expansions: implications for pathogenesis of fat redistribution
Fessel, W. J., S. E. Follansbee, et al. (2002), Aids 16(13): 1785-9.
Abstract: OBJECTIVE: To demonstrate relationships between plasma high-density lipoprotein (HDL) cholesterol and fat expansions in the fat redistribution syndrome. DESIGN: Patients who had significant buffalo humps or intra-abdominal fat (IAF) expansions were identified and their HDL levels were measured. Control patients were all those undergoing a single trial of antiretroviral treatment. Some patients answered a self-administered questionnaire concerning self-perceived fat expansions, and their responses were related to their HDL levels. In other patients, relationships were studied between IAF measured by cross-section computerized tomography scans and HDL levels. Finally, patients who had IAF > 70 cm(2), were administered niacin, 3000 mg/day for > or = 6 months, in order to test whether raising HDL induced a decrease in IAF. RESULTS: Twenty-three patients with buffalo humps had mean HDL of 30.4 mg/dl; 47 HIV-positive controls had mean HDL of 41.9 mg/dl (P = 0.001). In 27 patients, IAF area and HDL were negatively correlated (r, 0.40; P = 0.04). Among these 27, the 17 patients with IAF area > 100 cm(2) had mean HDL of 35.3 mg/dl; the 10 patients with IAF area < 100 cm(2) had mean HDL of 51 mg/dl (P < 0.05). The 24 patients who indicated in a questionnaire that they had self-perceived IAF expansion had a median HDL of 36.0 mg/dl; the 20 who indicated that they did not have IAF expansion had a median HDL of 44.5mg/dl (P = 0.06). IAF decreased by 26.9% in 13 (81%) of the 16 patients who took niacin for 1 year; and the decrease in IAF was associated with a significant (P = 0.002) increase in HDL.

High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered
Friedl, K. E., C. J. Hannan, Jr., et al. (1990), Metabolism 39(1): 69-74.
Abstract: We examined the influence of aromatization of testosterone on serum high-density lipoprotein cholesterol (HDL-C) and postheparin plasma hepatic triglyceride lipase activity (HTLA) in men. Eighteen healthy lean nonsmokers (ages, 20 to 33) were administered androgens in a weekly total dose of 280 mg for 12 weeks in one of three groups: testosterone enanthate (TE) (280 mg/wk intramuscularly IM); TE (280 mg/wk IM) + testolactone (TL) (250 mg orally PO four times daily); or methyltestosterone (MeT) (20 mg PO twice daily). Serum testosterone achieved steady state levels by 4 weeks with greater than 40 nmol/L (TE and TE + TL) and less than 15 nmol/L (MeT) while 17b-estradiol (E2) rose to greater than 250 pmol/L (TE) or remained below 70 pmol/L (TE + TL and MeT). LH fell to less than 5 U/L (TE and TE + TL) but remained unchanged with MeT. By 4 weeks, HDL-C had decreased significantly from 1.20 +/- 0.13 to 0.77 +/- 0.13 mmol/L (MeT), from 1.18 +/- 0.15 to 0.89 +/- 0.13 mmol/L (TE TL), and demonstrated no decrease in the TE group across the time course of the study. These changes were preceded by mean increases in HTLA of 102% (MeT) and 55% (TE + TL) over baseline, and no significant change with TE. The changes in HDL-C and HTLA returned to baseline within 2 weeks of steroid cessation. There were no changes in total cholesterol, triglycerides, or insulin in any group but, in the MeT group, apo AI levels decreased and low-density lipoprotein cholesterol (LDL-C) increased.(ABSTRACT TRUNCATED AT 250 WORDS)

High-density lipoprotein cholesterol is related to the TaqIB cholesteryl ester transfer protein gene polymorphism and smoking, but not to moderate alcohol consumption in insulin-dependent diabetic men
Dullaart, R. P., B. J. Beusekamp, et al. (1998), Scand J Clin Lab Invest 58(3): 251-8.
Abstract: In non-diabetic subjects, the high-density lipoprotein (HDL) cholesterol level is increased by alcohol and decreased by smoking. The biallelic B1B2 polymorphism of the cholesteryl ester transfer protein (CETP) gene is a genetic determinant of HDL cholesterol. We evaluated the effect of moderate alcohol consumption, the CETP gene polymorphism and clinical variables on HDL cholesterol and other lipoprotein parameters in insulin-dependent diabetic (IDDM) men. Thirteen moderate alcohol using IDDM men (median alcohol consumption 17 g/d) and 13 abstainers, individually matched for the CETP gene polymorphism and clinical factors including smoking, were studied. HDL cholesterol, serum apo AI and serum CETP activity levels were very similar in alcohol users compared to abstainers (1.36 +/- 0.28 vs 1.36 +/- 0.36 mmol l-1, 1.71 +/- 0.31 vs 1.75 +/- 0.33 g l-1 and 134 +/- 27 vs 138 +/- 53 nmol l-1h-1, respectively, n.s. for all). No significant differences in apo B-containing lipoproteins were observed. Multiple regression analysis (multiple r = 0.68) showed that HDL cholesterol was positively associated with the presence of the B2 allele (0.23 mmol l-1 higher for each B2 allele present, p = 0.004) and negatively with smoking (0.15 mmol l-1 lower per 10 cigarettes smoked daily, p = 0.011), but not with alcohol consumption (p = 0.66). This study suggests that moderate alcohol consumption has no beneficial effect on the lipoprotein profile in IDDM men. HDL cholesterol is adversely influenced by smoking, whereas considerable variation in its level appears to be explained by the CETP gene polymorphism.

High-density lipoprotein cholesterol levels and cholesterol efflux: a missing link?
Lorkowski, S. and P. Cullen (2004), Curr Opin Lipidol 15(1): 81-4.

High-density lipoprotein cholesterol strongly discriminates between healthy free-living and disabled octo-nonagenarians: a cross sectional study. Associazione Medica Sabin
Zuliani, G., E. Palmieri, et al. (1997), Aging (Milano) 9(5): 335-41.
Abstract: Aging is frequently associated with a deterioration in health and functional status, which often induces important modifications in several biological parameters, including plasma lipids; as a consequence, the real "meaning" of lipoprotein parameters in old individuals is complex. A cross sectional study was carried out in order to investigate the lipoprotein profile in very old individuals with or without disability, and evaluate the possible influence of other biological variables on plasma lipids. One hundred selected healthy free-living (FL) and 62 disabled (DIS) subjects aged over 80 were enrolled; 91 healthy adults matched for origin were included as controls. Lipoprotein profile total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, apoprotein A-I and B, anthropometric parameters, and ADL were measured. The FL octo-nonagenarians featured higher HDL-cholesterol levels than adult controls. DIS octo-nonagenarians showed lower total and HDL-C levels than FL. Discriminant analysis indicated that HDL-cholesterol and apoprotein A-I, but not total cholesterol, strongly discriminated between FL and DIS octo-nonagenarians. Multivariate analysis demonstrated that the waist/hip ratio, an index of visceral adiposity, was negatively associated with HDL-C levels in FL, but not in DIS elderly. We conclude that: 1) in very old individuals, the absence or presence of disability is strongly associated with high or low HDL-cholesterol values, respectively; 2) HDL-C and apo A-I are the parameters which better discriminate between FL and DIS octo-nonagenarians; and 3) the differences in HDL-C levels between FL and DIS are not due to modifications in anthropometric parameters. Prospective studies are needed to better understand the relationship between high-density lipoprotein levels, disability and aging.

High-density lipoprotein cholesterol, plasma triglyceride, and coronary heart disease: pathophysiology and management
Patsch, W. and A. M. Gotto, Jr. (1995), Adv Pharmacol 32: 375-426.

High-density lipoprotein cholesterol. Recommendations for routine testing and treatment
Lavie, C. J., J. H. O'Keefe, et al. (1990), Postgrad Med 87(7): 36-44, 47, 51.
Abstract: Evidence from epidemiologic, lipid intervention, and coronary angiographic studies demonstrates the importance of high-density lipoprotein cholesterol (HDL-C) in coronary artery disease (CAD) risk. Data from these studies strongly support the measurement of HDL-C in all patients screened for CAD. Patients with low levels should be treated using nonpharmacologic measures. High-risk patients deserve consideration for specific drug treatment.

High-density lipoprotein cholesterol: an updated view
Gotto, A. M., Jr. (2001), Curr Opin Pharmacol 1(2): 109-12.
Abstract: New insights into low high-density lipoprotein cholesterol identify promising new directions for coronary heart disease prevention. The ATP-binding-cassette A1 gene has been identified as an important defect in genetic disorders of this lipid fraction. Recent studies indicate a benefit in treating patients with low levels of high-density lipoprotein cholesterol and suggest new clinical recommendations.

High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: results from the MIRACL trial
Olsson, A. G., G. G. Schwartz, et al. (2005), Eur Heart J 26(9): 890-6.
Abstract: AIMS: Patients with acute coronary syndrome (ACS) in the Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study had diminished cardiovascular events after 16 weeks of treatment of atorvastatin 80 mg daily. We determined whether plasma lipoproteins at baseline and then at 6 weeks after randomization predicted clinical outcome. METHODS AND RESULTS: Cox proportional hazards models were constructed to determine relations between lipoproteins and clinical endpoint events. Baseline LDL cholesterol (LDL-C) did not predict outcome. In contrast, baseline HDL-C predicted outcome with a hazard ratio of 0.986 per mg/dL increment in HDL-C, P<0.001, indicating 1.4% reduction in risk for each 1 mg/dL increase in HDL-C. Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C. Neither Week 6 LDL-C nor absolute change of LDL-C from baseline by Week 6 had any significant impact on clinical endpoints occurring between Week 6 and Week 16 after randomization. CONCLUSION: Plasma HDL-C, but not LDL-C, measured in the initial stage of ACS predicts the risk of recurrent cardiovascular events over the ensuing 16 weeks. LDL-C reduction does not account for the clinical risk reduction with atorvastatin treatment after ACS. This finding may suggest that the clinical benefit of atorvastatin after ACS is mediated by qualitative changes in the LDL particle and/or by non-lipid (pleiotropic) effects of the drug.

High-density lipoprotein-cholesterol, its subfractions, and responses to exercise training are dependent on endothelial lipase genotype
Halverstadt, A., D. A. Phares, et al. (2003), Metabolism 52(11): 1505-11.
Abstract: Plasma high-density lipoprotein cholesterol (HDL-C) levels are an important independent risk factor for cardiovascular disease (CVD) that can be modified through exercise training. However, levels of HDL-C and its subfractions and their response to standardized exercise training are highly variable among individuals. Such variability suggests that levels of HDL-C, its subfractions, and their response to exercise training may be influenced by genetic variation and the interaction of that genetic variation with physical activity. The endothelial lipase gene (LIPG) may influence HDL-C metabolism and has several recently identified genetic variants. We hypothesized that the LIPG Thr111Ile polymorphism would be associated with variation in HDL-C levels and its subfractions and their response to exercise training. Eighty-three sedentary, healthy 50- to 75-year-old subjects were weight-maintained on an American Heart Association Step 1 Diet and then studied before and after aerobic exercise training. Sample size varied according to outcome measure as complete data was not available for all subjects. Initial age, body composition, and maximum oxygen consumption (V02max) did not differ between LIPG genotype groups (CC, n=41 to 44; CT/TT, n=37 to 39). Initial total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels were not significantly different between groups. The CT/TT group had lower initial HDL(2NMR)-C (12 +/- 1.0 v 17 +/- 1.1 mg/dL; P =.002) and integrated HDL(1,2NMR)-C (13 +/- 1.0 v 18 +/- 1.1 mg/dL; P=.002) levels and somewhat higher initial levels of integrated HDL(3,4,5)-C (31 +/- 2.2 v 25 +/- 2.3 mg/dL; P=.06). With exercise training, Vo2max increased, and body weight, total body fat, and visceral adipose tissue decreased similarly in both groups. With training, HDL-C levels increased twice as much (4.4 +/- 0.8 v 1.9 +/- 0.9 mg/dL; P=.04), HDL3-C levels increased almost 2-fold greater (3.8 +/- 0.7 v 2.2 +/- 0.6 mg/dL; P=.07), and HDL(5NMR)-C levels increased more than 4 times as much (2.2 +/- 0.8 v 0.5 +/- 0.6 mg/dL; P=.08) in the CC compared to the CT/TT group. We conclude that the LIPG genotype is associated with interindividual variability in HDL-C and its subfractions and their response to exercise training.

High-density lipoprotein-cholesterol: determining hygienic factors for intervention
Anzalone, D. A., F. L. Anzalone, et al. (1995), J Occup Environ Med 37(7): 856-61.
Abstract: Current guidelines of the Adult Treatment Panel on High-Density Lipoprotein-Cholesterol (HDL-C) emphasize the protective effect of HDL-C in reducing one's risk for coronary heart disease and recommend that individuals with serum HDL-C levels below 35 mg/dL utilize hygienic means to raise them. A cross-sectional study was performed to examine the relationship of the hygienic factors obesity (measured by percent body fat and body mass index), smoking, and aerobic exercise to HDL-C. The sample, consisting of 1701 male employees of a large aerospace hardware assembly plant, were evaluated by health risk appraisal and anthropometric measurement. Regression analysis revealed a significant negative relationship between body mass index, percent body fat, age, smoking and the level of HDL-C in the blood. Alcohol consumption was directly related to HDL-C, and Whites had a lower HDL-C than all other races combined. Aerobic exercise was not found to be significantly related to HDL-C. A model (multiple R2 =.1136) consisting of age, race, alcohol consumption, smoking, and body mass index fit the data well. These findings justify weight management and smoking cessation interventions for raising HDL-C. However, the role of aerobic exercise was not supported in this study as a means of raising HDL-C. Future studies should use maximum oxygen consumption as a measure of aerobic capacity, which may be a better indicator of aerobic exercise level. The role of medication and genetic and dietary factors in HDL-C management should also be explored. Although findings from this study support smoking cessation and weight management interventions, longitudinal research is needed to determine the most effective strategy for HDL-C management.

High-density lipoproteins from human alcoholics exhibit impaired reverse cholesterol transport function
Rao, M. N., Q. H. Liu, et al. (2000), Metabolism 49(11): 1406-10.
Abstract: We have previously shown that chronic alcohol consumption leads to inhibition of sialylation of apolipoprotein E (apo E) that results in its impaired binding to high-density lipoprotein (HDL) molecule. Because apo E plays a major role in reverse cholesterol transport (RCT), we speculated that ethanol-mediated formation of HDL molecules without apo E may affect the RCT process. Therefore, we have investigated whether the RCT function of HDL is affected in chronic alcoholics with or without liver disease compared with nondrinkers. HDL was isolated from fasting plasma of normal subjects, n = 9 (nondrinkers), chronic alcoholics, n = 8 (ALC), and chronic alcoholics with liver disease, n = 6 (ALD). A portion of HDL sample from each subject was evaluated for its cholesterol efflux capacity from 3Hcholesterol oleate preloaded mouse macrophages. The remaining portion of each HDL sample was labeled with 3Hcholesterol oleate and evaluated for its ability to deliver cholesterol to the liver using HepG2 cells in culture. Cholesterol efflux capacity of HDLs was decreased by 83% (P <.0002) in alcoholics without liver disease and by 84% (P <.0006) in alcoholics with liver disease compared with the HDLs from nondrinkers. The capacities of HDLs to deliver cholesterol to the liver were decreased by 54% (P <.005) in alcoholics without liver disease and by 64% (P <.005) in alcoholics with liver disease compared with the HDLs from nondrinkers. The fact that further complications by liver disease in alcoholic subjects did not significantly exacerbate the extent of impairment in RCT function of HDL suggest that alcohol per se is responsible for its deleterious effects on RCT. Significantly, plasma HDL apo E concentration relative to that of apo A1 (apo E/apo A1 ratio) was also decreased by 31% to 32% (P <.0005) in alcoholics without or with liver disease compared with nondrinkers. It is therefore concluded that chronic alcohol consumption adversely affects the RCT function of HDL by altering its association with apo E due to ethanol-induced desialylation of apo E.

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