Marked hyper-HDL2-cholesterolemia associated with premature corneal opacity. A case report

We report here a peculiar case with premature corneal opacity and extremely high levels of HDL cholesterol in serum. The patient is a 54-year-old man who was first noticed to have marked corneal opacities at age 19. His serum HDL cholesterol level was elevated to the level of 135-160 mg/dl, while total serum cholesterol and triglyceride concentrations were 254 mg/dl and 56 mg/dl, respectively. Serum apoprotein A-I and E levels analyzed by single radial immunodiffusion method were elevated in the case. Serum lipoprotein fractions isolated by preparative ultracentrifugation revealed that increased levels of HDL cholesterol were accounted for solely by the HDL2 fraction. HDL2 of the patient contained relatively higher amounts of apoprotein E than normal control HDL2. Elution profiles of lipoproteins in high performance liquid chromatography revealed that HDL2 particles from the patient were larger in size than those from normal controls. These characteristics of HDL are in part similar to those of HDLC which appears in experimental animals after cholesterol feeding. Such abnormalities in HDL2 fractions associated with premature corneal opacity have not been reported so far and appear to constitute a new disease entity.     

High density lipoprotein metabolism in endurance athletes and sedentary men

BACKGROUND. Endurance athletes have higher high density lipoprotein (HDL) concentrations than sedentary controls. To examine the mechanism for this effect, we compared HDL apoprotein metabolism in 10 endurance athletes aged 34 +/- 6 years (mean +/- SD) and 10 sedentary men aged 36 +/- 8 years. METHODS AND RESULTS. Subjects were maintained on controlled diets for 4 weeks, and metabolic studies using autologously labeled 125I HDL were performed during the final 2 weeks. Lipids and lipoproteins were measured daily during these 2 weeks, and the average of 14 values was used in the analysis. HDL cholesterol (58 +/- 14 versus 41 +/- 10 mg/dl), HDL2 cholesterol (26 +/- 10 versus 12 +/- 8 mg/dl), and apolipoprotein A-I (apo A-I) (144 +/- 18 versus 115 +/- 22 mg/dl) were higher in the athletes, whereas triglyceride concentrations (60 +/- 18 versus 110 +/- 48 mg/dl) were lower (p less than 0.01 for all). Postheparin lipoprotein lipase activity was not different, but hepatic triglyceride lipase activity was 27% lower (p less than 0.06) in the athletes. The athletes' mean clearance rate of triglycerides after an infusion of Travamulsion (1 ml/kg) was nearly twofold that of the inactive men (5.8 +/- 1.5 versus 3.2 +/- 0.9%/min, p less than 0.001). There was no differences in HDL apoprotein synthetic rates, whereas the catabolic rates of both apo A-I (0.15 +/- 0.02 versus 0.22 +/- 0.05 pools per day, p less than 0.01) and apolipoprotein A-II (apo A-II) (0.15 +/- 0.02 versus 0.20 +/- 0.04 pools per day, p less than 0.05) were reduced in the trained men. Apo A-I and apo A-II half-lives correlated with HDL cholesterol in each group (r greater than 0.76, p less than 0.05 for all) but not consistently with lipase activities or fat clearance rates. This relation between apoprotein catabolism and HDL cholesterol was strongest at HDL cholesterol concentrations of less than 60 mg/dl. CONCLUSIONS. We conclude that higher HDL levels in active men are associated with increased HDL protein survival. The mechanisms mediating this effect require better definition, and other factors appear to contribute to HDL cholesterol and protein concentrations among individual subjects.     

Serum lipoprotein lipid and apoprotein levels as indicators of the severity of angiographically assessed coronary artery disease

Serum lipoprotein cholesterol and triglycerides and apoproteins A-I, A-II and B were determined in 71 consecutive male subjects undergoing coronary angiography because of severe angina pectoris. Among the factors studied, apoprotein B, apoprotein B/A-I ratio, VLDL- and LDL cholesterol showed the most consistent association with the severity of coronary artery disease as assessed by angiography whereas serum HDL cholesterol and apoproteins A-I and A-II showed no correlation. Subjects with stenosis of the left main coronary artery had higher serum HDL cholesterol and apoprotein A-I and B levels than the others. In this series which comprised males with severe angina pectoris, derived from a population with high prevalence of coronary heart disease, LDL was the best indicator of the severity of coronary artery disease.     

Lipid and apoprotein modifications in body builders during and after self-administration of anabolic steroids

To determine the effects of anabolic steroids on serum lipid and apoprotein levels, 14 white male body builders who self-administered steroids for 2 to 3 months (steroid users) were studied; 10 agreed to screening while they were taking the drugs (ON treatment) and also at about 3 months following their suspension (OFF treatment). Controls consisted of 17 body builders who had never taken steroids (nonusers), and a group of 18 healthy sedentary subjects (controls). During the period of steroid administration, there was a slight reduction in total serum cholesterol, with a marked cholesterol decrease in the high-density lipoprotein (HDL) subfractions HDL2 and HDL3, and a significant reduction in the HDL2 cholesterol/HDL3 cholesterol ratio; the percentage of serum cholesterol transported by low-density lipoproteins (LDL) increased significantly. In addition, a marked apoprotein (apo) A-I reduction in the HDL2 and HDL3 subfractions was observed, as well as an apo A-II decrease that was significant only in the HDL3 subfraction, with an A-I/A-II ratio significantly reduced in both subfractions. Serum apo B was only slightly increased, with a very high B/A-I ratio. Apolipoprotein C-II and E levels showed no modifications, while apo C-III reduced significantly. Lipid and apoprotein values returned to almost normal levels in the OFF treatment period. Findings in the group of nonusers were similar to those in sedentary subjects. These results indicate that anabolic steroids profoundly alter the serum lipid-protein profile, and the changes may be caused in part by the significant differences observed in apoprotein levels.     

Variation in susceptibility to atherosclerosis among inbred strains of mice

The effect of short-term exercise withdrawal on plasma lipoproteins, apoprotein A-I (Apo A-I), and lecithin:cholesterol acyltransferase (LCAT) was studied in moderately trained lifestyle exercisers. Eight endurance-trained men, age 18-45 years (means = 29 years), withdrew from aerobic activity for 6 weeks, while an age and fitness-matched control group (n = 9) maintained normal exercise habits. A baseline period that included two blood samplings preceded the detraining intervention. Plasma total cholesterol (TCHOL), HDL cholesterol (HDL-C) and triglyceride (TG) levels were determined weekly. Other blood variables (HDL2-C, HDL3-C, Apo A-I, and LCAT), % fat, and aerobic capacity (VO2max) were measured pre-, mid-, and post-experiment. A two-way repeated measures analysis of variance (ANOVA) indicated that the 6-week exercise withdrawal period failed to elicit significant mean changes in any blood variable, % fat, or VO2max. Therefore, a short-term layoff from aerobic activity by moderately trained, chronic exercisers generally does not adversely affect the blood lipoprotein profile or aerobic capacity.     

Association of hypertensive status and its drug treatment with lipid and haemostatic factors in middle-aged men: the PRIME study

Aims: To assess the association of hypertensive status and antihypertensive drug treatment with lipid and haemostatic levels in middle-aged men.Methods and results: Hypertensive status, antihypertensive drug treatment, total and high-density lipoprotein (HDL) cholesterol, triglyceride, apoproteins A-I and B, lipoparticles LpA-I, LpE:B and Lp(a), fibrinogen, plasminogen activator inhibitor-1 (PAI-1) activity and factor VII were assessed in a sample of men 50-59 years living in France (n = 7050) and Northern Ireland (n = 2374). After adjustment for age, body mass index, smoking status, educational level, country, alcohol drinking and hypolipidaemic drug treatment, untreated hypertensive subjects had higher levels of total cholesterol, triglyceride, apoproteins A-I and B and PAI-I activity than normotensive subjects. On univariate analysis, diuretics decreased total and HDL-cholesterol and apoproteins A-I and B; those differences remained after multivariate adjustment. Treatment with beta-blockers decreased total and HDL-cholesterol, apoprotein A-I and LpA-I, and this effect remained after multivariate adjustment. Calcium channel blockers decreased total cholesterol and apoproteins A-I and B; those differences remained significant after multivariate adjustment. ACE inhibitors decreased total cholesterol, triglycerides, apoprotein B and LpE:B; and this effect remained after multivariate adjustment. Analysis of the subjects on monotherapy showed beta-blockers to decrease total cholesterol and HDL parameters and angiotensin-converting enzyme (ACE) inhibitors to decrease low-density lipoprotein (LDL)-related parameters, while no effect was found for the other antihypertensive drugs.Conclusions: Hypertensive status is associated with an unfavourable lipid and haemostatic profile in middle-aged men. Antihypertensive treatment with beta-blockers decreases HDL parameters, whereas treatment with ACE inhibitors appears to decrease total cholesterol and LDL-related parameters.     

Long-term exercise training with constant energy intake. 3: Effects on plasma lipoprotein levels

The composition and concentration of plasma lipoproteins were studied in five young men (mean BMI = 27.5 +/- 2.9 (s.d.] before, during (after 25 and 50 days of training), and after the completion of a 100 day exercise training program that induced daily 4.2 MJ calorie deficit. Along with reductions in body weight (from 86.7 +/- 20.0 to 78.7 +/- 17.1 kg, P less than 0.01) and in fat mass (from 17.0 +/- 9.7 to 10.4 +/- 7.4 kg, P less than 0.01), the exercise training program induced numerous changes in plasma lipoprotein levels. Plasma total cholesterol level fell significantly after 25 days of training (P less than 0.05) and remained significantly reduced at the end of the training experiment (P less than 0.05). This reduction in total plasma cholesterol was accompanied by reductions in plasma apoprotein (apo) B, LDL-cholesterol and LDL-apo B levels (P less than 0.05). There were trends for reductions in plasma triglyceride and VLDL components that were significant only for VLDL-triglycerides (P less than 0.05). Plasma HDL-cholesterol levels increased significantly only at the end of the training program (P less than 0.01). This increase in plasma HDL-cholesterol was not accompanied by an increase in plasma apo A-I levels suggesting that exercise training produced an increase in HDL cholesterol content rather than an increase in HDL particle number. Ratios of HDL-cholesterol/cholesterol (P less than 0.01) and apo A-I/apo B (P less than 0.05) were significantly increased by exercise training, suggesting a decreased risk of cardiovascular disease. These results indicate that a reduction in fat mass solely induced by aerobic exercise training has substantial beneficial effects on plasma lipoprotein levels.     

Relationships of plasma estradiol, testosterone, and sex hormone-binding globulin with lipoproteins, apolipoproteins, and high density lipoprotein subfractions in men

Plasma estradiol, testosterone, and sex hormone-binding globulin (SHBG) were studied in relation to plasma lipoproteins, high density lipoprotein (HDL) subfractions, and apolipoproteins in 73 healthy but sedentary middle-aged men. Among potentially confounding variables, a strong positive association was found between estradiol levels and cigarette use, while testosterone and SHBG correlated negatively with percent body fat and alcohol intake. After adjustment for smoking, percent body fat, and alcohol, plasma estradiol levels correlated negatively with total cholesterol and low density lipoprotein cholesterol, and testosterone levels correlated positively with apolipoprotein B, while SHBG levels correlated positively with HDL2 mass and apolipoprotein A-I. SHBG was also strongly associated with the waist to hip girth ratio (WHR). Adjustment for WHR eliminated the significant associations of SHBG with triglycerides, HDL2 mass, and apolipoprotein A-I. SHBG levels and WHR may reflect tissue sensitivity and the impact of exposure to fluctuating levels of sex hormones for a period of days, or longer. These variables may provide more insight into the role of sex hormones in lipoprotein metabolism than do single samples of circulating hormones. It is also suggested that long term effects of sex hormones on adipose tissue distribution may at least partially underlie sex-related differences in lipoprotein metabolism.     

Relationship of the phenotypic expression of the A-IMilano apoprotein with plasma lipid and lipoprotein patterns

The plasma lipoprotein and apolipoprotein profile of 29 adult A-IMilano (A-IM) carriers and 29 age- and sex-matched non-affected subjects of the same kindred was examined, in order to investigate linkages between the lipid and apoprotein abnormalities and the phenotypic expression of the biochemical disorder. Carriers (A-IM+) showed a higher prevalence of hypertriglyceridemia (12 out of 29); they also had lower plasma total cholesterol, esterified cholesterol and phospholipids, compared to non-carriers. Lipoproteins were characterized by a significant enrichment of triglycerides in low and high density fractions (LDL and HDL), and by the expected striking reduction of HDL mass and cholesterolemia. Conversely, no significant alterations of the major circulating apolipoprotein levels, except for apo A-I and apo A-II, were noted in the A-IM+. The increased free cholesterol/esterified cholesterol ratio in plasma (most marked in HDL), was accompanied by a significant reduction of the lecithin cholesterol acyl transferase molar activity. Several correlations pertaining to lipids, lipoproteins and apoproteins were examined: cholesterol and triglycerides in HDL and, more remarkably, apoprotein A-I and C-III levels in plasma were significantly correlated in the A-IM+. While there was no significant prevalence of specific apo E phenotypes, plasma triglycerides and apo C-II levels were highly correlated in the carriers. The A-IM subjects, while in the presence of severe lipoprotein risk factors, may have alternative mechanisms of cholesterol disposal, potentially responsible for the apparently low prevalence of atherosclerosis.     

Differential effects of continuous versus intermittent administration of growth hormone to hypophysectomized female rats on serum lipoproteins and their apoproteins

The effects of the plasma pattern of GH on serum and lipoprotein levels of total cholesterol, triglycerides, apolipoprotein A-I (apo A-I), apolipoprotein B 48/100 (apo B), and apolipoprotein E (apo E) were studied in hypophysectomized female Sprague-Dawley rats, which had been given replacement therapy with L-T4 and hydrocortisone. Bovine GH (1 mg/kg.day) was administered sc either continuously by means of osmotic minipumps or by two daily injections. Serum lipoproteins were separated by sequential ultracentrifugation into very low density lipoproteins [density (d) less than 1.006 g/ml], low density lipoproteins (LDL; d 1.006-1.063 g/ml) and high density lipoproteins (HDL; d 1.063-1.21 g/ml). The content of total cholesterol and triglycerides were then determined. Apo A-I, apo B, and apo E were isolated from rat serum and antibodies raised in rabbits. In serum and in lipoprotein fractions, the content of apo A-I, apo-B, and apo E were determined by electroimmunoassay. After hypophysectomy, there occurred a decrease in serum cholesterol and serum levels of apo A-I and apo E, in spite of replacement therapy with T4 and cortisone. Similar changes were also observed in HDL. In contrast, apo B, cholesterol, and triglycerides were increased in LDL. Estradiol treatment had no effect on these changes. Continuous infusion of GH resulted in an increase in cholesterol and apo E in serum and HDL to the levels of intact females. In contrast, GH given twice daily had no effect. Therefore, the sexually dimorphic secretion of GH may be important for the regulation of sex differences in apo E and HDL cholesterol levels. There were no consistent effects of GH treatment on the levels of apo A-I in serum or HDL, but GH treatment resulted in a decrease in apo B and triglycerides in both serum and LDL, regardless of the mode of administration. This suggests that GH regulates the serum and LDL levels of apo B and triglycerides independently of the secretory pattern.     

Increased concentration of high density lipoprotein in plasma and decreased platelet aggregation in primary biliary cirrhosis

Plasma lipoprotein concentration and composition were studied in 7 female patients with primary biliary cirrhosis and compared with 6 normal, age-matched controls. The effect of the lipoproteins derived from these patients on the function of normal platelets was also tested. High levels of plasma cholesterol and phospholipids and a raised free/esterified cholesterol ratio were found. In 4 of the patients, both HDL cholesterol and HDL protein were increased, and high levels of plasma apoprotein A-I and A-II were evident. This abnormal HDL did not contain excess apolipoprotein E. The VLDL and LDL fractions were also abnormal, as evidenced by a high cholesterol/protein ratio. Little correlation between lipoprotein disorders and clinical condition was found. Platelet function was reduced in all patients. LDL from the patients reduced aggregation of normal platelets, whereas HDL had a minimal effect. The abnormal lipoproteins in these patients may contribute to their abnormal in vitro platelet aggregation.     

A study of the lipid transport system in the cat, Felix domesticus

Feline serum lipoproteins were fractionated into four distinct classes by density gradient ultracentrifugation and characterized with respect to physical and chemical properties. The distribution of serum lipids, lipoproteins and apolipoproteins was quite unlike that in man, the cat having five times as much high density lipoproteins (HDL) as low density lipoproteins (LDL). The lipoproteins in the d less than 1.019 g/ml fraction of cats were larger and were richer in triglycerides than their human counterparts and contained a considerable amount of beta-migrating particles. The low density lipoproteins of cats and man had similar chemical composition, but cat LDL had a higher negative charge, were smaller and contained apoprotein A-I. Cat HDL consisted of two distinct subfractions HDL2 and HDL3 with similar density boundaries and particle size as in man. In cat serum and HDL fraction apoprotein A-II was a minor component. Like human serum, fasting cat serum contained only the larger species of apoprotein B, apo B-100, whereas intestinal lymph contained exclusively the smaller apo B-48. Post heparin feline and human plasma possessed both lipoprotein lipase and hepatic lipase. Chylomicrons formed after a fat load in cats were removed from the circulation as rapidly as in man. It is concluded, that the cat is another animal model of potential interest for the study of lipoprotein metabolism.     

Prevalence of serum lipid abnormalities in chronic hemodialysis.

Fasting levels of serum triglyceride, cholesterol, high-density lipoprotein (HDL), apoprotein A-I, HDL cholesterol, and HDL triglyceride were measured in 94 uremic males receiving maintenance hemodialysis and 6 uremic males receiving chronic peritoneal dialysis. These patients had higher serum triglyceride levels (p less than 0.001) and lower cholesterol levels (p less than 0.001) than normal controls. The dialysis patients treated with androgen or propranolol and those who were hypothyroid or diabetic had significantly higher triglyceride levels than the other dialysis subjects. The dialysis patients who had no additional secondary causes of hypertriglyceridemia had abnormalities in HDL; in comparison to normals and triglyceride-matched controls, these patients had elevated HDL triglyceride levels and low HDL cholesterol levels, despite similar HDL apoprotein A-I levels. The HDL cholesterol levels appeared to be lower in those patients than could be accounted for by their degree of hypertriglyceridemia.     

Serum phospholipid transfer protein activity and genetic variation of the PLTP gene.

The inverse relationship between serum levels of high density lipoproteins (HDL) and risk of coronary heart disease is well established. The phospholipid transfer protein (PLTP) promotes the transfer of phospholipids between lipoproteins and modulates HDL size and composition. It thus plays a central role in HDL metabolism. Serum PLTP activity was measured in 400 healthy Finnish individuals in order to determine normal PLTP serum values. PLTP activity increased with age (P<0.001), so that the PLTP activity was 3.81+/-0.84 micromol/ml per h (mean +/- S.D., n = 52) for men and 3.97+/-0.11 micromol/ml per h (n = 52) for women in the youngest age group (25-35 years), while it was 6.77+/-0.17 micromol/ml per h (n = 45) for men and 6.68+/-0.15 micromol/ml per h (n = 40) for women in the oldest age group (56-65 years). PLTP activity correlated significantly (P<0.001) with body mass index (r = 0.22), serum total cholesterol (r = 0.17), the ratio of HDL-cholesterol/total cholesterol (r = -0.20), triglycerides (r = 0.20), apo A-II (r = 0.20), and gamma glutamyl transferase (r = 0.22) values. Serum PLTP activity correlated negatively (r = -0.20, P<0.001) with levels of apolipoprotein A-I in HDL particles that contained only apo A-I [Lp(A-I) particles]. The allelic frequencies of six intragenic polymorphisms, -79G/T, -56G/A, -37T/C, -31A/G, Phe2Leu, Arg121Trp, and two neutral polymorphisms, located in the immediate vicinity of the PLTP gene were determined. There were no significant associations between these polymorphisms and serum PLTP activity.     

Type III hyperlipoproteinemia: rise in high-density lipoprotein levels in response to therapy.

The experience of the Washington University Lipid Research Center in the treatment of type III hyperlipoproteinemia is reported. Six women and seven men were prescribed a type III diet and/or clofibrate over periods of two to eight months. Mean total plasma cholesterol and triglyceride levels declined by 51 and 74 per cent, respectively, whereas mean levels of high-density lipoprotein (HDL) cholesterol rose from 34 to 50 mg/dl (p < 0.001). Rises in HDL cholesterol levels were seen in every subject, whereas levels of HDL triglycerides fell. Plasma concentrations of apolipoproteins (Apo) A-I and A-II, which make up 90 per cent of the protein moieties of the HDL, were also measured for the first time in the patients with type III hyperlipoproteinemia by radioimmunoassay. Levels of both apoproteins rose with therapy (from 83 to 108 mg/dl and from 35 to 43 mg/dl, respectively, p < 0.02 for both). The sums of triglyceride + cholesterol in the HDL, + A-I + A-II in plasma, were increased by therapy from 170 to 211 mg/dl (p < 0.05). There was a significant negative correlation between the change in HDL cholesterol and the change in very low-density lipoprotein (VLDL) triglyceride (r = ? 0.720; p < 0.01). Low-density lipoprotein (LDL) (density (d) 1.006 to 1.063 g/ml) cholesterol remained unchanged but LDL triglycerides decreased. Therefore, both the levels and compositions of the low- and high-density lipoproteins were affected by therapy. Levels of cholesterol and triglycerides in the d < 1.006 g/ml lipoproteins both decreased but without changes in their ratios. Visible regression of xanthomas occurred in six of six patients. Intermittent claudication and angina pectoris diminished in five of five and two of two patients, respectively. Thus, alterations in plasma lipoproteins were associated with clinical improvement. It is not known which of the changes in lipoproteins were most beneficial—the lowering of the d < 1.006 class, which is directly related to high coronary risk, or the elevation of high-density lipoproteins, which are inversely related to risk. Perhaps both contributed to the unique responsiveness of clinical signs and symptoms to therapy in patients with type III hyperlipoproteinemia.     

Effect of postpartum lactation on lipoprotein lipids and apoproteins

To determine if postpartum lactation alters plasma lipoprotein lipid and apoprotein concentrations and composition, we studied 56 overnight fasting lactating and 16 nonlactating women approximately 6 weeks postpartum. Postpartum results are presented as absolute concentrations and as the difference from antepartum values determined at 36 weeks gestation. Antepartum lipoprotein lipid and apoprotein concentrations were generally not different in the 2 groups, with the single exception of whole plasma and low density lipoprotein (LDL) apoprotein (apo) B (probably a chance difference). When expressed as the antepartum and postpartum difference, the lactating and nonlactating groups were indistinguishable in very low density lipoprotein (VLDL) and LDL triglyceride, cholesterol, phospholipid, and apo B concentrations. However, lactating women had higher high density lipoprotein (HDL) cholesterol, phospholipid, apo A-I, and apo A-II concentrations than nonlactating women when results were expressed as differences from antepartum values or as absolute values. HDL triglyceride concentrations were not significantly different between lactating and nonlactating women by either analysis. There was no significant effect of lactation on VLDL or LDL composition, but there was a significant increase in the percent cholesterol content in HDL. We hypothesize that the increase in HDL constituents in lactation is generated in part by increased catabolism of triglyceride-rich lipoproteins by the lactating breast.     

Quantitation of apolipoprotein A-I of human plasma high density lipoprotein.

High density lipoproteins (HDL) may be controlled via their major apolipoprotein, A-I. To study this apolipoprotein, a simple, precise, and accurate immunodiffusion assay for A-I was developed and applied in a sample of Bell Telephone Company employees. A-I showed a slight increase with age in men (r=0.11, n=263) and women (r=0.15, n=257). A-I correlated closely with HDL cholesterol (r=0.72). It was weakly related to total triglyceride in women (r=0.24) but was inversely related in men (r=-0.17). Women on estrogen had the highest A-I levels (149 mg/dl +/- 26, x +/- S.D., n=29, p is less than 0.05), followed by women on combination oral contraceptives (141 +/- 26, n=80) whereas women on no medication had lower levels (129 +/- 25, n=99, p is less than 0.01) but men had the lowest levels (120 +/- 20, p is less than 0.01) In a separate group of 14 women given estrogen for 2 wks (1 mug/kg/day), A-I increased by 24%. Thus A-I is increased by exogenous and, most likely, endogenous estrogen, Among hyperlipidemic referral subjects, those with hypercholesterolemia (n=43) and hypertriglyceridemic women (n=33) had normal A-I levels. Among hypertriglyceridemic men both A-I and HDL cholesterol values were decreased (115 +/- 20, p is less than 0.01 and 37 +/- 3, p is less than 0.01, respectively, n=68) but were significantly lower among a group of myocardial infarction survivors (107 +/- 16, p is less than 0.01, and 27 +/- 6, p is less than 0.01, respectively, n=24). High density lipoprotein levels and the content of cholesterol in HDL associated with A-I appear to be decreased in coronary heart disease.     

Plasma High-Density Lipoproteins and Liver Lipids and Proteins in Man

ABSTRACT. The association of high-density lipoproteins (HDL) in plasma with liver lipids and proteins was investigated in 28 subjects with diagnostic liver biopsy. Lipids and proteins were evaluated in relation to hepatic histology and microsomal enzyme induction, assessed by liver cytochrome P-450. Moderate-severe hepatic parenchymal changes were associated with low liver phospholipids, protein and cytochrome P-450, low plasma HDL cholesterol (HDL-C), and high hepatic triglycerides. Liver microsomal induction accompanying anti-convulsant therapy was associated with high liver phospholipids and protein, high plasma HDL-C, apoproteins A-I and A-II, and high HDL-C/total cholesterol (T-C) ratio. HDL-C, A-I and the HDL-C/T-C ratio were directly proportional to liver phospholipids, protein and cytochrome P-450, inversely related to hepatic triglycerides. Increases in hepatic phospholipids and protein, characteristic of microsomal induction, may lead to the elevation of plasma HDL apoprotein and HDL-C levels and HDL-C/T-C ratios, and thus reduce the risk of coronary heart disease.     

Associations of resting heart rate with concentrations of lipoprotein subfractions in sedentary men

In major prospective studies it has been reported that high heart rate at rest predicts the development of coronary heart disease (CHD) or cardiovascular disease (CVD) in men, but the mechanisms producing these relationships are unknown. Since lipoprotein levels contribute strongly to the risk of CHD and CVD, we examined the relationship of resting heart rate to plasma concentrations of high-density (HDL), low-density (LDL), and very low-density (VLDL) lipoproteins, apolipoprotein (apo) A-I and A-II, and serum concentrations of lipoprotein subfractions in 81 men to determine if atherogenic lipoproteins could potentially induce the reported association of heart rate with development of CHD or CVD. The significant (p less than or equal to .05) Spearman's correlations for resting heart rate vs HDL2 mass (rs = -.24), HDL3 mass (rs = -.40), HDL cholesterol (rs = -.36), apo A-I (rs = -.29), triglycerides (rs = .31), VLDL cholesterol (rs = .24), VLDL mass (rs = .27), and LDL mass of Sof 0-7 subfraction (rs = .30) lend support to our hypothesis of lipoprotein-induced relationships of CHD with heart rate. The correlations for resting heart rate vs triglycerides, HDL cholesterol, HDL3 mass, VLDL mass, and LDL mass of Sof 0-7 subfraction remain significant when adjusted for adiposity, age, smoking habits, diet, and physical fitness as measured by maximum aerobic power (VO2 max) or submaximal heart rate during a graded exercise test.     

Effect of alcohol intake and exercise on plasma high-density lipoprotein cholesterol subfractions and apolipoprotein A-I in women

Abstinence from alcohol consumption for 3 weeks was followed by 3 weeks of wine intake in 18 inactive and 18 physically active premenopausal women (runners). The runners weighed less and had higher plasma high-density lipoprotein (HDL) cholesterol and lower low-density lipoprotein cholesterol levels than the inactive women. There were no differences between groups in plasma total cholesterol, triglyceride and apolipoprotein A-I concentrations. Runners had higher plasma HDL2 cholesterol concentrations than inactive women (34 +/- 17 vs 19 +/- 12 mg/dl), but HDL3 cholesterol concentration did not differ between the groups (41 +/- 10 vs 39 +/- 9 mg/dl). Addition of 35 g/day of ethanol for 3 weeks did not result in a significant change in either group for any of the variables measured. The amount of exercise appears to be a more important determinant of plasma lipoproteins and apolipoprotein A-I than alcohol intake in premenopausal women.