Concentrations of high-density lipoprotein subfraction HDL2 and lipoprotein A-I in a random population of healthy subjects

1991 ◽  
Vol 37 (12) ◽  
pp. 2111-2113 ◽  
Author(s):  
D Roche ◽  
M L Migueres ◽  
N T Lequang ◽  
M Burstein ◽  
O G Ekindjian ◽  
...  
Keyword(s):  
Low Cost ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Strongly Correlated ◽  
Lipoprotein A ◽  
The Difference ◽  
Apoprotein Composition ◽  
Hdl2 Cholesterol

Abstract High-density lipoproteins (HDL) are now currently subdivided according either to density and size—HDL2 and HDL3—or to surface apoprotein composition—lipoprotein A-I (LpA-I) without A-II, and LpA-I:A-II. In samples from blood bank donors (60 women, 47 men), we evaluated HDL subclasses, LpA-I particles, and other classic risk factors for atherosclerosis and compared them with each other. We found a good correlation between HDL2 and LpA-I (r = 0.74, P < 0.001), the correlation being more marked in women (r = 0.74) than in men (r = 0.67). LpA-I was also strongly correlated with total apolipoprotein A-I (apoA-I) (r = 0.61), which suggests that LpA-I represents a significant portion of the variable pool of apoA-I. By contrast, LpA-I:A-II but not LpA-I was correlated with HDL3, confirming the preferential association of LpA-I with HDL2. The difference between the sexes was more marked for HDL2 (+66% in women) than for LpA-I (+25%). We conclude that in normolipemic subjects the size of the HDL2 pool depends on that of LpA-I. Considering the speed and low cost of the assay, determination of HDL2 cholesterol might be a useful tool for assessing cardiovascular risk.

Determination of high-density lipoprotein phospholipids in serum.

1980 ◽  
Vol 26 (9) ◽  
pp. 1275-1277 ◽  
Author(s):  
Y Yamaguchi
Keyword(s):  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mean Value ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Color Development ◽  
The Mean

Abstract I describe a method for measuring high-density lipoprotein phospholipids. Magnesium chloride and dextran sulfate are used to precipitate all low-density and very-low-density lipoproteins. The supernate contains only high-density lipoproteins, the phospholipid concentration of which is determined by an enzymic method. The precision of the method (CV) is 2.35% (10 repeated assays), and the mean value for HDL-phospholipids was 1006 (SD 248) mg/L for 30 apparently healthy subjects. I used electrophoresis and enzymic color development to confirm the presence of HDL-phospholipids. Results are compared with those obtained by an ultracentrifugation method.

Fetal and Maternal Lipoprotein Metabolism in Human Pregnancy

1995 ◽  
Vol 88 (3) ◽  
pp. 311-318 ◽  
Author(s):  
Richard H. Neary ◽  
Mark D. Kilby ◽  
Padma Kumpatula ◽  
Francis L. Game ◽  
Deepak Bhatnagar ◽  
...  
Keyword(s):  
Caesarean Section ◽  
High Density Lipoprotein ◽  
Cholesteryl Ester ◽  
Free Cholesterol ◽  
Cholesterol Metabolism ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lipoprotein A ◽  
Lipid Enrichment

1. Lipid, apolipoprotein concentration and composition were determined in maternal venous and umbilical arterial and venous blood at delivery by elective Caesarean section in 13 full-term pregnancies and in 25 healthy non-pregnant females. The indications of Caesarean section were a previous Caesarean section or breech presentation. None of the women was in labour and there were no other complications of pregnancy or fetal distress. 2. The objectives of the study were to establish whether the placenta has a role in feto-maternal cholesterol metabolism through either synthesis or transplacental cholesterol flux. The potential for free cholesterol diffusion between mother and fetus and rates of cholesterol esterification and transfer between lipoproteins were determined and related to the differences in composition between fetal and maternal lipoproteins. 3. Pregnant women had raised levels of all lipid and lipoprotein fractions compared with control subjects. The greatest increases were in free cholesterol and triacylglycerol (P < 0.0001). Lipoprotein (a) levels were significantly greater in the pregnant women [112(12.2) mg/l] than in the control women [50 (10.0) mg/l]. 4. The only significant correlation between maternal and fetal lipoprotein concentrations was in lipoprotein (a) levels (r = 0.791, P = 0.002). In both umbilical venous and arterial blood, concentrations of very-low- and low-density lipoproteins, particularly apolipoprotein B, cholesteryl ester and triacylglycerol, were lower than in maternal blood (P < 0.0001), but high-density lipoprotein levels were similar. 5. There was no umbilical arteriovenous differences in lipoprotein concentration or composition. This suggests that cholesterol synthesis or free cholesterol diffusion does not occur in the placenta. The relative concentrations of free cholesterol to phospholipid in maternal and fetal lipoproteins do not indicate the existence of a concentration gradient favouring free cholesterol diffusion across the placenta. 6. The esterification of free cholesterol was significantly reduced in maternal [17.7 (2.4) μmol h−1 l−1, P < 0.001] and fetal [6.7 (3.5) μmol h−1 l−1, P < 0.0001] compared with control [40.9 (13.2) μmol h−1 l−1] blood. 7. In fetal compared with maternal high-density lipoproteins the ratios cholesteryl ester/apoliproprotein A-I [0.84 (0.35) versus 0.40 (0.05), P < 0.01] and phospholipid/apolipoprotein A-I [1.66 (0.14) versus 0.58 (0.10), P < 0.0001] indicated lipid enrichment of these particles in the fetus. 8. Lipid enrichment of high-density lipoprotein is due in part to a marked reduction in transfer of cholesteryl ester in the fetus [1.0 (0.6) μmol h−1 l−1] compared with maternal [6.15 (1.3) μmol h−1 l−1, P = 0.004] and control [17.3 (7.2) μmol h−1 l−1, P < 0.0001] blood. 9. In conclusion, there was no evidence for involvement of the placenta in cholesterol metabolism during pregnancy. In fetal life high-density lipoproteins are lipid rich, partly because of a reduction in transfer of esterified cholesterol to other particles. Maternal and fetal lipoprotein levels are not correlated, although the results suggested that lipoprotein (a) levels may be related.

Enzymatic determinations of cholesterol in high-density-lipoprotein fractions prepared by a precipitation technique.

1976 ◽  
Vol 22 (1) ◽  
pp. 98-101 ◽  
Author(s):  
B W Steele ◽  
D F Koehler ◽  
M M Azar ◽  
T P Blaszkowski ◽  
K Kuba ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Total Cholesterol ◽  
Convenient Method ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lipid Research ◽  
Enzymatic Method ◽  
Fine Precipitate

Abstract An enzymatic method for cholesterol in serum [Clin. Chem. 20, 470 (1974)] was initially found to be unsatisfactory for measuring cholesterol in high-density-lipoprotein fractions prepared by precipitation with Mn2+. A fine precipitate formed in the cuvette and cholesterol values were falsely increased. We describe a simple, convenient method for circumventing these problems. An ethylenediaminetetraacetate solution is used to reconstitute the enzymatic reagent. Cholesterol values by this procedure correlated with those obtained by the Lipid Research Clinic's procedure for the same lipoprotein fraction preparations (regression slope, .998; Y-intercept, 8.9 mg/liter; correlation coefficient, .984; standard error of the estimate, 16.8 mg/liter). Precision of the assay, including the precipitation step, was calculated. The SDwithin day was 9.7 mg/liter and SDoverall was 23.7 mg/liter. Results for total cholesterol with the modified reagent were linearly related to concentrations exceeding 4 g/liter, thereby permitting determination of high-density-lipoproteins and total cholesterol in a single run.

Composition of serum very-low-density and high-density lipoproteins in diabetes.

1980 ◽  
Vol 26 (9) ◽  
pp. 1261-1265 ◽  
Author(s):  
J Gabor ◽  
M Spain ◽  
N Kalant
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Cholesterol Content ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Protein Ratio ◽  
Apolipoprotein Ciii ◽  
Apoprotein Composition

Abstract We examined the cholesterol/protein ratio and the apoprotein composition of serum lipoproteins in a randomly selected population of maturity-onset diabetics and in a group of nondiabetics of similar age. We found no differences in cholesterol distribution between the groups as a whole, but diabetics with above-normal low-density lipoproteins (LDL) had decreased concentrations of high-density lipoprotein (HDL) cholesterol. In the diabetics as a whole, there was an increase in the cholesterol/protein ratio in HDL, a negative correlation between the amounts of LDL cholesterol and HDL cholesterol, an increase in the proportion of apolipoprotein C in very-low-density lipoprotein (VLDL), and a decrease in the proportion of the apolipoprotein AI component of HDL. In diabetic subjects with increased VLDL, there was an increase in the relative amount of apolipoprotein CIII, and a consequent decrease in the ratio of apolipoprotein CII/apolipoprotein CIII in the VLDL. In both diabetic and control subjects, apolipoprotein E and cholesterol content of VLDL were linearly related.

Use of a dual-precipitation procedure for measuring high-density lipoprotein 3 (HDL3) in normolipidemic serum.

1989 ◽  
Vol 35 (7) ◽  
pp. 1390-1393 ◽  
Author(s):  
T A Cloey ◽  
P S Bachorik
Keyword(s):  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
Cholesterol Concentration ◽  
Precipitation Method ◽  
Serum Samples ◽  
Precipitation Procedure ◽  
The Difference ◽  
Hdl2 Cholesterol

Abstract We compared results by a dual-precipitation method (J Lipid Res 1982;23:1206-23) for measuring high-density lipoprotein 3 (HDL3) cholesterol with those by ultracentrifugation at d 1.125, using 56 fresh and 105 frozen-stored serum samples. For both methods, HDL2-cholesterol was calculated as the difference between total HDL-cholesterol and HDL3-cholesterol. In general, for pooled serum samples, agreement was closest with ultracentrifugation when we used a dextran sulfate concentration of 5.0 mg/L to precipitate the HDL2-rich fraction, although the optimal concentration varied from 3.0 to 6.8 mg/L for different pools. For individual samples, the values for HDL3 by dual precipitation averaged 12.8% lower than by ultracentrifugation. The coefficients of correlation between the two methods were HDL3, r = 0.70; and HDL2, r = 0.92. The dual-precipitation method reflected the expected sex-related differences in HDL2-cholesterol concentration and inverse relationship with triglyceride concentration.

Flow-cytometric determination of high-density-lipoprotein binding sites on human leukocytes.

1987 ◽  
Vol 33 (12) ◽  
pp. 2195-2203 ◽  
Author(s):  
G Schmitz ◽  
G Wulf ◽  
T Brüning ◽  
G Assmann
Keyword(s):  
Binding Sites ◽  
Rapid Determination ◽  
Gradient Centrifugation ◽  
Density Lipoprotein ◽  
Cell Types ◽  
High Density ◽  
High Density Lipoproteins ◽  
Nonspecific Binding ◽  
Surface Binding

Abstract In this method, leukocytes were isolated from 6 mL of EDTA-blood by density-gradient centrifugation and subsequently incubated with rhodamine isothiocyanate (RITC)-conjugated high-density lipoproteins (HDL). The receptor-bound conjugate particles were determined by fluorescent flow cytometry and compared with 125I-labeled HDL binding data for the same cells. Human granulocytes express the highest number of HDL binding sites (9.4 X 10(4)/cell), followed by monocytes (7.3 X 10(4)/cell) and lymphocytes (4.0 X 10(4)/cell). Compared with conventional analysis of binding of 125I-labeled HDL in tissue-culture dishes, the present determination revealed significantly lower values for nonspecific binding. In competition studies, the conjugate competes for the same binding sites as 125I-labeled HDL. With the use of tetranitromethane-treated HDL3, which fails to compete for the HDL receptor sites while nonspecific binding is not affected, we could clearly distinguish between 37 degrees C surface binding and specific 37 degrees C uptake of RITC-HDL3, confirming that the HDL receptor leads bound HDL particles into an intracellular pathway rather than acting as a "docking" type of receptor. Patients with familial dysbetalipoproteinemia showed a significantly higher number of HDL binding sites in the granulocyte population but normal in lymphocytes and monocytes, indicating increased uptake of cholesterol-containing lipoproteins. In patients with familial hypercholesterolemia, HDL binding was increased in all three cell types, indicating increased cholesterol uptake and increased cholesterol synthesis. The present method allows rapid determination of HDL binding sites in leukocytes from patients with various forms of hyper- and dyslipoproteinemias.

A study of the use of polyethylene glycol in estimating cholesterol in high-density lipoprotein.

1980 ◽  
Vol 26 (13) ◽  
pp. 1775-1779 ◽  
Author(s):  
P N Demacker ◽  
A G Hijmans ◽  
H E Vos-Janssen ◽  
A van't Laar ◽  
A P Jansen
Keyword(s):  
Polyethylene Glycol ◽  
High Density Lipoprotein ◽  
Reference Values ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
High Density Lipoproteins ◽  
Polyethylene Glycol 6000

Abstract We studied polyethylene glycol 6000 precipitation of lipoproteins other than high-density lipoproteins, before cholesterol is estimated in the supernate. Other lipoproteins in the supernatant fractions were detected by using rocket immunoelectrophoresis. A polyethylene glycol concentration of 75 g/L in the final mixture appeared to be optimal, and results agreed with those obtained by ultracentrifugation. Differences in serum pH, use of polyethylene glycol from different suppliers, or the presence of ethylenediaminetetraacetate resulted in values that differed significantly (by 40 to 60 mumol/L) from the reference values. Polyethylene glycol did not interfere in four different methods for determination of cholesterol. In combination with an enzymic cholesterol method, the polyethylene glycol method appeared to be very precise, even when lipemic sera (triglycerides up to 5.5 mmol/L) were analyzed that had diminished high-density lipoprotein cholesterol values. We consider this method a method of choice, especially when lipemic sera are tested and enzymic cholesterol analysis is used.

scholarly journals High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad and the Future

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 857
Author(s):  
Josep Julve ◽  
Joan Carles Escolà-Gil
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
Epidemiological Studies ◽  
High Density ◽  
High Density Lipoproteins ◽  
Atherosclerotic Cardiovascular Disease ◽  
Plasma High Density ◽  
Low Levels

Epidemiological studies have shown that low levels of plasma high-density lipoprotein cholesterol (HDL-C) are associated with increased atherosclerotic cardiovascular disease (CVD) [...]

scholarly journals High-Density Lipoproteins and the Kidney

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 764
Author(s):  
Arianna Strazzella ◽  
Alice Ossoli ◽  
Laura Calabresi
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Cholesterol Acyltransferase ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lcat Deficiency ◽  
Progression Of Renal Disease ◽  
The Impact

Dyslipidemia is a typical trait of patients with chronic kidney disease (CKD) and it is typically characterized by reduced high-density lipoprotein (HDL)-cholesterol(c) levels. The low HDL-c concentration is the only lipid alteration associated with the progression of renal disease in mild-to-moderate CKD patients. Plasma HDL levels are not only reduced but also characterized by alterations in composition and structure, which are responsible for the loss of atheroprotective functions, like the ability to promote cholesterol efflux from peripheral cells and antioxidant and anti-inflammatory proprieties. The interconnection between HDL and renal function is confirmed by the fact that genetic HDL defects can lead to kidney disease; in fact, mutations in apoA-I, apoE, apoL, and lecithin–cholesterol acyltransferase (LCAT) are associated with the development of renal damage. Genetic LCAT deficiency is the most emblematic case and represents a unique tool to evaluate the impact of alterations in the HDL system on the progression of renal disease. Lipid abnormalities detected in LCAT-deficient carriers mirror the ones observed in CKD patients, which indeed present an acquired LCAT deficiency. In this context, circulating LCAT levels predict CKD progression in individuals at early stages of renal dysfunction and in the general population. This review summarizes the main alterations of HDL in CKD, focusing on the latest update of acquired and genetic LCAT defects associated with the progression of renal disease.

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