Showing papers on "High-density lipoprotein published in 1979"
TL;DR: It is suggested that HDL cholesterol is an independent risk factor for CHD, especially in males over 50, and the implication is that increased HDL cholesterol might play a protective role in the pathogenesis of CHD.
Abstract: Using univariate and multivariate analyses, the association between high density lipoprotein (HDL) cholesterol and coronary heart disease (CHD) incidence was investigated. Over 150 cases of myocardial infarction (MI) occurred among 6500 Israeli adult males in a five-year prospective study. At age 50 years and over, there is a significant inverse association between MI incidence and HDL cholesterol. This relationship persists when controlling for risk factors such as age, other cholesterol components, smoking, blood pressure, weight, and diabetes mellitus. Unlike hypercholesterolemia and smoking, the relative risk with HDL cholesterol increases with age above 50. Similar patterns of association occur between HDL cholesterol and angina pectoris incidence, sudden unexpected death and deaths from MI. It is suggested that HDL cholesterol is an independent risk factor for CHD, especially in males over 50, and the implication of this study is that increased HDL cholesterol might play a protective role in the pathogenesis of CHD.
266 citations
TL;DR: The recent finding of increased lipoprotein lipase activity in adipose tissue and muscle of endurance runners suggests that increased lipolytic rate of trigly ceride-rich lipoproteins may be an initial step in a sequence of events leading to higher plasma levels of HDL2.
Abstract: The influence of vigorous activity in man on plasma lipids and lipoproteins is reviewed, with particular emphasis on high density lipoproteins. Both cross sectional and longitudinal (or training) studies have been reported, many of them of less than ideal design. Nonetheless, a consistent pattern emerges in which increased exercise levels lead to lower plasma concentrations of triglycerides and very low density lipoproteins, and of low density lipoproteins. High density lipoprotein levels increase. Sometimes, but not uniformly, plasma total cholesterol level falls as the result of these changes. The increase in plasma high density lipoprotein appears to be the result largely of an increase in the less dense HDL2 subfraction. Plasma apolipoprotein A-I levels (but not apo-A-II levels) seem to increase concomitantly. The precise biochemical mechanism responsible for these changes has not been elucidated; but the recent finding of increased lipoprotein lipase activity in adipose tissue and muscle of endurance runners suggests that increased lipolytic rate of trigly ceride-rich lipoproteins may be an initial step in a sequence of events leading to higher plasma levels of HDL2.
256 citations
TL;DR: The data suggest that the effects of nicotinic acid on the HDL subfraction distribution may be mediated via (a) net transfer of ApoA-I from HDL(3) to HDL(2) and (b) a reduction in ApOA-II synthesis.
Abstract: This report describes the effects of pharmacologic doses (3 g/d) of nicotinic acid on the plasma distribution and chemical composition of the high density lipoprotein (HDL) subfractions HDL2 and HDL3 and examines the influence of the drug on the metabolism of the major HDL apoproteins, apolipoproteins A-I (ApoA-I) and A-II (Apo-II).
The drug lowered plasma cholesterol (15%, P < 0.05) and triglyceride (27%, P < 0.01); the former effect a result of a fall in the amount of cholesterol associated with very low density lipoproteins (31%, P < 0.02) and low density lipoproteins (36%, P < 0.02). Conversely, it raised plasma HDL cholesterol (23%, P < 0.05) and increased (by 345%) the plasma HDL2:HDL3 ratio. The latter derived from an absolute increment (646%) in circulating HDL2, coupled with a fall (47%) in HDL3. This change was not associated with major alterations in the overall cholesterol (free and esterified), triglyceride, phospholipid, or protein content of the subfractions; however, it was accompanied by substantial changes in their protein composition. In particular, the molar ratio of ApoA-I:ApoA-II in HDL3 declined from 2.7:1 to 2.1:1 during nicotinic acid treatment.
Significant perturbations of ApoA-I and ApoA-II metabolism accompanied the drug-induced HDL subfraction redistribution. Specifically, the plasma concentration of ApoA-I rose by 7% (P < 0.05) because of a decrease in its fractional catabolic rate. Moreover, whereas before treatment 6 and 94% of the plasma ApoA-I circulated with HDL2 and HDL3, after commencement of nicotinic acid therapy this distribution became 49 and 51% in HDL2 and HDL3, respectively. ApoA-II was found mainly in HDL3, both before and during nicotinic acid treatment. Administration of the drug caused a 14% reduction in its plasma concentration (P < 0.05), which derived principally from a fall (22%, P < 0.01) in its synthetic rate.
These data suggest that the effects of nicotinic acid on the HDL subfraction distribution may be mediated via (a) net transfer of ApoA-I from HDL3 to HDL2 and (b) a reduction in ApoA-II synthesis. Our present understanding of the association between HDL and atherosclerosis indicates that such changes may have prophylactic value in the prevention of coronary artery disease.
248 citations
TL;DR: Vicious regular walking resulted in a reduction of body fate stores, endogenous insulin requirements, and food intake, and perhaps improved the ability to eliminate cholestrol by increasing the plasma high density lipoprotein fraction.
219 citations
TL;DR: The availability of this anti-hepatic lipase serum offered a good opportunity to study the function of the enzyme by searching whether plasma lipoproteins are influenced by specific inhibition of the hepatic endothehal lipase in vivo.
216 citations
TL;DR: Some lipid and lipoprotein accompaniments of obesity and its association with glucose intolerance are examined in the Framingham cohort of 5209 men and women ages 30 to 59 examined biennially over 18 years.
203 citations
TL;DR: It is suggested that low levels of HDL cholesterol are important risk factors for the development of atherosclerosis and that they may be useful for identifying patients at high risk of certain anatomic patterns of coronary artery disease.
Abstract: Epidemiologic studies have found associations between low levels of high density lipoprotein (HDL) cholesterol and increased risk of coronary artery disease, using myocardial infarction or angina pectoris as endpoints. However, since most studies have not correlated HDL cholesterol with the presence, severity, or location of anatomically proven coronary disease, the present study measured HDL cholesterol levels in 483 men and women undergoing coronary arteriography. Consistent and statistically significant trends of decreasing mean HDL cholesterol levels with increasing numbers of diseased coronary arteries were observed in both men and women and in younger and older age groups. Although women without coronary disease had much higher levels of HDL cholesterol than men without coronary disease, the differences between men and women with similar degrees of coronary disease were small. Low levels of HDL cholesterol were associated with left main coronary disease; patients with both triple vessel disease and left main disease had lower levels of HDL cholesterol than did patients with triple vessel disease without left main disease. These results were not explained by the possible associations of low density lipoprotein cholesterol or triglycerides with HDL cholesterol. These findings suggest that low levels of HDL cholesterol are important risk factors for the development of atherosclerosis and that they may be useful for identifying patients at high risk of certain anatomic patterns of coronary artery disease.
159 citations
TL;DR: Long-term colestipol and diet treatment reduced the xanthoma size and stabilized serially angiographically visualized atherosclerotic lesions in 21 of the 25 patients who showed a satisfactory hypolipemic response and did not cause nutritional or metabolic disturbances.
Abstract: Long-term effects of diet and colestipol (a bile acid sequestrant) were studied in 25 patients with familial type II hyperlipoproteinemia. Serum lipids and body weights of an initial group of 30 patients were stabilized by low cholesterol-saturated fat-refined carbohydrate diet and the patients were then randomized into placebo and drug-treatment groups. After explaining that the drug is nontoxic and effective in lowering serum lipids, total cholesterol (C) and low-density lipoprotein cholesterol (LDL-C), colestipol (30 g/day) and diet were given to the 25 patients who remained in the long-term follow-up program. The treatment resulted in highly significant lowering of serum lipids (mg/dl, mean +/- SEM): C and LDL-C from 412.7 +/- 24.4 and 331.1 +/- 22.8 to 270 +/- 11.0 and 188.1 +/- 13.8, respectively (p less than 0.001 in each instance) over 7--7 1/2 years. Although we observed no absolute increase in high density lipoprotein (HDL), the HDL/LDL ratio was elevated. Long-term colestipol and diet treatment reduced the xanthoma size and stabilized serially angiographically visualized atherosclerotic lesions in 21 of the 25 patients who showed a satisfactory hypolipemic response. It did not cause nutritional or metabolic disturbances.
137 citations
TL;DR: Lower prevalence of IHD in women with FH is suggested in due to their higher concentration of HDL-cholesterol, which is not only similar to that in men with IHD, but is also significantly lower than the level observed in Women with tendinous xanthomas but no IHD.
130 citations
TL;DR: There was a direct correlation (r=0.86, p<.001) between mean HDL-cholesterol and triglyceride levels, and the progrestin effect was studied here in more detail in two women with type V hyperlipoproteinemia treated with norethindrone acetate.
Abstract: High density lipoprotein (HDL) levels are known to be higher in women than in men, and to increase with estrogen use. To assess the effects of estrogens on HDL subspecies, analytic ultracentrifuge measurements of HDL were compared in 11 menopausal estrogen users and 16 controls. The difference in mean schlieren patterns between the groups showed a significantly higher level of HDL with flotation rate (F 1.20 o )>1.5 (predominantly HDL2) in the users. This was similar to the difference in HDL seen between nonusers of hormones and age-matched males. A previous study had shown that users of combination oral contraceptives had increased levels of HDL with F 1.20 o ≤3.5 (primarily HDL3) suggesting that the estrogen effect on HDL is altered by the presence of added progestin. The progrestin effect was studied here in more detail in two women with type V hyperlipoproteinemia treated with norethindrone acetate. Reduction in serum triglyceride was accompanied by a reduction in HDL, predominantly in the less dense species (HDL2). Among groups of oral contraceptive and noncontraceptive estrogen and progestin users whose HDL-cholesterol levels have been reported recently, there was a direct correlation (r=0.86, p<.001) between mean HDL-cholesterol and triglyceride levels. Endogenous hormonal influences on HDL were assessed by serum hormone and lipoprotein measurements at weekly intervals during two consecutive menstrual cycles in four healthy females. An increase in HDL of highest flotation rate (F 1.20 o 5–9) was seen, which corresponded with the time of ovulation raising the possibility of pituitary as well as gonadal hormone effects on HDL.
104 citations
Journal Article•
TL;DR: The present prospective study confirms that HDL cholesterol is inversely associated with the risk of developing CHD in middle-aged men.
Abstract: The high density lipoprotein (HDL) cholesterol concentrations of frozen specimen obtained in 1972-73 are reported from 93 men aged 40-49 years who later developed coronary heart disease (CHD), and for 186 controls. Mean HDL cholesterol of CHD-patients was 7.9% lower than that of controls matched for smoking habits and serum concentrations of triglycerides and total cholesterol (p 0.05 for 82 men who had myocardial infarction, n.s. difference for 11 with sudden coronary death), and 10.2% lower (p 0.05) than that of controls who were not matched for the parameters mentioned. The present prospective study confirms that HDL cholesterol is inversely associated with the risk of developing CHD in middle-aged men.
TL;DR: These studies suggest that the detergent may achieve its hyperlipidemic effct by disrupting HDL and thus removing the A-I and C-II proteins from a normal activating environment compirsing VLDL, HDL, and the enzymes.
TL;DR: Data from simultaneous radiolabeled very low density lipoprotein and HDL studies in 2 individuals are consistent with the concept that apoC-II and apo C-III are catabolized at a different rate than are apoA-I and apOA-II within the HDL density range.
Abstract: The composition and metabolism of high density lipoprotein (HDL) subfractions were investigated in seven nomal individuals. Mean HDL2 (d, 1.063–1.125 g/ml) composition (by weight) was 43% protein, 28% phospholipid, 23% cholesterol, and 6% triglyceride, and mean HDL3 (d, 1.125–1.21 g/ml) composition was 58% protein, 22% phospholipid, 14% cholesterol, and 5% triglyceride. The mean apoA-I; apoA-II weight ratio was 4.75 for HDL2 and 3.65 for HDL3.HDL2 protein was proportionally slightly richer in C apolipoproteins and higher molecular weight constituents (including apoE) than HDL3. Kinetic studies utilizing radiolabeled HDLA (d, 1.09–1.21 g/ml), HDL2, and HDL3 demonstrated rapid exchange of apoA-I and apoA-II radioactivity among HDL subfractions, similar fractional rates of catabolism of apoA-I and apoA-II within HDL, and similar radioactivity decay within HDL subfractions. Mean plasma residence time was 5.74 days for radiolabeled HDL2 and 5.70 days for radiolabeled HDL3. Differences in HDL protein mass among individuals were largely due to alterations in catabolism, and in general both HDL2 and HDL3 were catabolized via a plasma and a nonplasma pathway. Data from simultaneous radiolabeled very low density lipoprotein and HDL studies in 2 individuals are consistent with the concept that apoC-II and apoC-III are catabolized at a different rate than are apoA-I and apoA-II within the HDL density range.
TL;DR: The results demonstrate the cholestyramine treatment affects HDL metabolism in a way which, according to current concepts, may prove beneficial to the recipient.
TL;DR: The number of solubilized receptors was 1/20th of normal in mutant fibroblasts from a subject with homozygous familial hypercholesterolemia and was 1-4th ofnormal in human epithelioid carcinoma A-431 cells when they were grown in the presence of 25-hydroxycholesterol plus cholesterol.
Abstract: The low density lipoprotein (LDL) receptor was solubilized from membranes of bovine adrenal cortex and cultured human cells by incubation with the nonionic detergent octyl-β-D-glucoside. Receptor activity released into the 100,000 × g supernatant was assayed by a solid-phase procedure: an aliquot of the soluble extract was removed, the detergent was diluted below its critical micellar concentration, causing the receptor to precipitate as a lipid—protein aggregate; the precipitate was collected by centrifugation and incubated with 125I-labeled LDL (125I-LDL); and the receptor-bound 125I-LDL was separated from free 125I-LDL by filtration. The 125I-LDL binding site that was precipitated from the soluble extract of bovine adrenocortical membranes appeared to be the same as the functional LDL receptor of cultured bovine adrenocortical cells and human fibroblasts. It exhibited high affinity and specificity (affinity for LDL more than 200-fold greater than for acetylated LDL, methylated LDL, or high density lipoprotein), dependence on calcium, and susceptibility to destruction by Pronase. The amount of 125I-LDL binding activity in solubilized membranes from cultured cells was proportional to the number of receptors on the surface of the intact cells. Thus, the number of solubilized receptors was 1/20th of normal in mutant fibroblasts from a subject with homozygous familial hypercholesterolemia and was 1/4th of normal in human epithelioid carcinoma A-431 cells when they were grown in the presence of 25-hydroxycholesterol plus cholesterol. While in the soluble form in the presence of octyl-β-D-glucoside, the LDL receptor can be carried through several steps of purification.
TL;DR: The results confirm recent reports of a raised HDL-C in those insulin-dependent diabetics who are prone to coronary heart disease.
TL;DR: A clearly significant increased HDL cholesterol has been demonstrated in the dieters as compared to well matched control subjects, and might be of interest in the view of HDL cholesterol as a well documented and independent "antirisk factor" for coronary heart disease.
TL;DR: It is indicated that certain plant fibers selectively lower plasma total cholesterol while raising high-density lipoprotein cholesterol levels in cholesterol-fed rats which received diets supplemented with 10% pectin, guar gum, or oat bran fiber.
Abstract: SummaryCholesterol-fed rats which received diets supplemented with 10% pectin, guar gum, or oat bran fiber showed a reduced accumulation of cholesterol and triglyceride in both plasma and the liver. In contrast, an increase in the plasma high-density lipoprotein cholesterol levels of these same rats was noted. This study indicates that certain plant fibers selectively lower plasma total cholesterol while raising high-density lipoprotein cholesterol levels.These studies were supported in part by Grant 1 RO1 AM 20889-01 from the National Institute of Arthritis, Metabolism and Digestive Diseases.
TL;DR: In sedentary subjects with coronary artery disease, a modest increase in activity can result in an increase in the HDL-C level and a decrease in the plasma insulin concentration, and these changes occurred in the absence of variations in diet, smoking habits, adiposity, or plasma triglyceride concentrations.
Abstract: The effects of a 13-week moderate exercise program on fasting plasma insulin, lipids, and lipoprotein cholesterol concentrations were studied in 32 sedentary, middle-aged men with coronary artery disease. The preponderant component of the exercise program was walking or slow jogging. There was no significant change in the systolic blood pressure and pulse rate product response to a standard exercise load. The high-density lipoprotein-cholesterol (HDL-C) level increased, and the fasting plasma insulin concentration decreased. There were no significant changes in plasma triglycerides or low-density lipoprotein cholesterol levels. In sedentary subjects with coronary artery disease, a modest increase in activity can result in an increase in the HDL-C level and a decrease in the plasma insulin concentration. These changes occurred in the absence of variations in diet, smoking habits, adiposity, or plasma triglyceride concentrations and did not require a cardiovascular training effect. ( JAMA 242:2190-2192, 1979)
TL;DR: The rapid rate of labelling of V LDL from HDL suggests that the transfer of HDL cholesteryl esters to VLDL may represent a significant pathway for the disposal of HDL cholesterol.
TL;DR: Observations indicate that the hyperlipidemia induced by estrogen administration is accompanied by marked alterations, both qualitative and quantitative, in the plasma lipoproteins.
Journal Article•
TL;DR: The findings of the present study suggest that the "retarding" effect of alcohol on coronary artery disease may be at least partially explained by the alcohol-induced rise of plasma HDL cholesterol.
TL;DR: The effects of chronic, oral dichloroacetate administration (as the sodium salt) in two patients with severe homozygous familial hypercholesterolemia markedly reduced serum total and low density cholesterol levels and lowered the low density lipoprotein to high density cholesterol ratio.
TL;DR: The lipoproteins isolated from rat plasma by flotation in the density range 1.019-1.063 g/ml were further characterized and lipoprotein HDL1 was notable for both the concentration of its esterified cholesterol, which was similar to that of LD lipop protein, and the low triacylglycerol content, resembling that of HD lipop Protein.
Abstract: The lipoproteins isolated from rat plasma by flotation in the density range 1.019-1.063 g/ml were further characterized. Using rate zonal ultracentrifugation, we isolated two lipoproteins in almost equal proportions from this density range. Similar isolations may be accomplished with density gradients in a swinging-bucket rotor. On isopycnic-density-gradient ultracentrifugation one component banded at rho = 1.031 g/ml and the other at rho = 1.054 g/ml. More that 98% of the apoprotein of the lighter component was B protein, and hence this particle is LD (low-density) lipoprotein. Of the apoproteins of the rho = 1.054 g/ml particles, designated lipoprotein HDL1, over 60% was arginine-rich peptide, and the remainder was A-I, A-IV and C peptides. The molecular weight of these lipoproteins determined by agarose column chromatography was 2.36 × 10(6) for LD lipoprotein and 1.30 × 10(6) for lipoprotein HDL1. On electron microscopy the radius of LD lipoprotein was 14.0 nm and that of lipoprotein HDL1 was 10.0 nm, in contrast with molecular radii of 10.4 nm and 8.4 nm respectively determined from the gel-permeation-chromatography data. The lipid and phospholipid composition of both particles was determined. Lipoprotein HDL1 was notable for both the concentration of its esterified cholesterol, which was similar to that of LD lipoprotein, and the low triacylglycerol content, resembling that of HD lipoprotein. The possible origin of lipoprotein HDL1 is discussed.
TL;DR: Fluctuations of HDL-C with time appear to be related in part to variations in triglyceride-rich lipoprotein metabolism, which needs to be taken into account when making comparisons in epidemiological studies of the predictive powers of single on-entry measurements for future disease.
TL;DR: The results suggest that there is no preferential removal of apo-C-II or apolipoprotein C-III-1 from lipolyzed VLDL particles, and indicate that the ratio of Apo- c-II to c-III does not regulate the extent of lipolysis of different VLDl particles, at least in V LDL isolated from normolipidemic humans.
TL;DR: A significant redistribution of cholesterol in lipoproteins following ingestion of large doses of D,L-alpha tocopherol (vitamin E) is documented, which includes cholesterol redistribution in favor of the HDL fraction, with decreases in very-low-density lipoprotein (VLDL) levels and total triglycerides.
Abstract: A significant redistribution of cholesterol in lipoproteins following ingestion of large doses of D, L-alpha tocopherol (vitamin E) is documented. In persons with decreased high-density lipoprotein (HDL) cholesterol a complex response occurs, which includes cholesterol redistribution in favor of the HDL fraction, with decreases in very-low-density lipoprotein (VLDL) levels and total triglycerides. The response was studied in five persons with average cholestrol distributions and five persons with cholesterol distributions associated with high risk of coronary heart disease. The mean elevation of the HDL cholesterol concentration in the former group was 168% of the initial value, while the latter group experienced post-therapy levels 375% of initial levels.
TL;DR: Graft function was sustained in 19 patients, in whom HDL-cholesterol and apo A concentrations increased to lie within normal limits by six months after the operation, and changes in HDL with successful kidney grafting augur well in a population with many risk factors for coronary heart disease.
Abstract: Serum high-density-lipoprotein (HDL) cholesterol and apoprotein (apo) A concentrations were significantly reduced at the time of renal transplantation in 26 patients with chronic renal failure. In a prospective evaluation the behaviour of HDL concentrations after grafting was found to depend on renal function. Graft function was sustained in 19 patients, in whom HDL-cholesterol and apo A concentrations increased to lie within normal limits by six months after the operation. Successful transplantation also restored to normal the lipid and protein content of HDL as expressed by the ratio of HDL cholesterol to apo A. When transplant function was not sustained (seven patients), however, no changes in HDL were observed up to the time of the graft loss. Such changes in HDL with successful kidney grafting augur well in a population with many risk factors for coronary heart disease.
TL;DR: Following infarction albumin and transferrin fell, alpha 2-macroglobulin did not change, and alpha 1-acid glycoprotein, caeruloplasmin, haptoglobin and IgM rose, which are probably part of the general metabolic response to trauma.