Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure

Gidez, Lewis I.; Miller, George; Burstein, M; Slagle, Susan; Eder, Howard A.

doi:10.1016/s0022-2275(20)38059-7

Cited by 711 publications

(17 citation statements)

References 48 publications

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“…Total serum cholesterol (TC), triglycerides and high density lipoprotein cholesterol (HDL-C) were measured using Boehringer diagnostic kits by an enzymatic colorimetric method. 13,14 HDL-C subfraction levels were measured after separation by the precipitation procedure of Gidez et al 15 Low density lipoprotein cholesterol (LDL-C) was estimated by calculation, using the Friedewald fomula. 16 Apolipoproteins, (apo) A-I and B were determined by radial immunodiffusion using agarose plaques.…”

Section: Laboratory Methodsmentioning

confidence: 99%

Lipid and lipoprotein levels in premenopausal systemic lupus erythematosus patients

Formiga¹,

Meco²,

Pintó³

et al. 2001

Lupus

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The purpose of this study was to assess the prevalence of dyslipoproteinemia and to analyze the clinical variables that are associated with it in a sample of premenopausal systemic lupus erythematosus (SLE) patients. We studied 53 premenopausal (34.5 y) SLE outpatients and 45 controls. Clinical variables studied included patient age, weight, height, body mass index (BMI), age at disease onset, disease duration, clinical activity of SLE, renal involvement and drug therapy. Total cholesterol (TC), high- and low-density lipoprotein cholesterol (HDL-C and LDL-C), and triglycerides were measured using standard enzymatic techniques. Apolipoproteins (apo) A-I and B were determined by radial immunodiffusion. Twenty-nine patients (55%) and 14 controls (30%) had dyslipoproteinemia. An increase in TC, triglycerides, HDL3-C, apo A-I and apo B, and a decrease in HDL2-C and HDL-C/TC index was found in SLE patients in comparison with controls. TC (P = 0.007), apo B (P = 0.02), LDL-C (P = 0.03) and triglycerides (P = 0.0001) were significantly correlated with proteinuria. Patients on prednisone therapy had higher triglycerides levels (P = 0.03) than untreated patients. TC (P = 0.01), LDL-C (P = 0.006) and triglycerides (P = 0.04) were also correlated with the dose of prednisone. Dyslipoproteinemia is a common feature in adult SLE premenopausal patients which is characterized by an increase in TC, triglycerides and apo B, and an abnormal distribution of HDL subclasses. Corticosteroid therapy and proteinuria are the best predictors of dyslipoproteinemia in these patients.

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Section: Laboratory Methodsmentioning

confidence: 99%

Lipid and lipoprotein levels in premenopausal systemic lupus erythematosus patients

Formiga¹,

Meco²,

Pintó³

et al. 2001

Lupus

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“…The HDL 2 and HDL 3 were isolated by double precipitation as described by Gidez et al (22). All apoB-containing lipoproteins were precipitated by mixing 1 mL of plasma with 0.1 mL of heparin-MnCl 2 .…”

Section: Laboratory Proceduresmentioning

confidence: 99%

Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase: high density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype

Mahley

Pépin

Palaogğlu

et al. 2000

Journal of Lipid Research

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Turks have strikingly low levels of high density lipoprotein cholesterol (HDL-C) (10-15 mg/dL lower than those of Americans or Western Europeans) associated with elevated hepatic lipase mass and activity. Here we report that Turks have low levels of high density lipoprotein subclass 2 (HDL 2 ), apoA-I-containing lipoproteins (LpA-I), and pre-␤ -1 HDL and increased levels of HDL 3 and LpA-I/A-II particles (potentially an atherogenic lipid profile). The frequency distributions of HDL-C and LpA-I levels were skewed toward bimodality in Turkish women but were unimodal in Turkish men. The apoE genotype affected HDL-C and LpA-I levels in women only. In women, but not men, the 2 allele was strikingly more prevalent in those with the highest levels of HDL-C and LpA-I than in those with the lowest levels. The higher prevalence of the 2 allele in these subgroups of women was not explained by plasma triglyceride levels, total cholesterol levels, age, or body mass index. The modulating effects of apoE isoforms on lipolytic hydrolysis of HDL by hepatic lipase (apoE2 preventing efficient hydrolysis) or on lipoprotein receptor binding (apoE2 interacting poorly with the low density lipoprotein receptors) may account for differences in HDL-C levels in Turkish women (the 2 allele being associated with higher HDL levels). In Turkish men, who have substantially higher levels of hepatic lipase activity than women, the modulating effect of apoE may be overwhelmed. The gender-specific impact of the apoE genotype on HDL-C and LpA-I levels in association with elevated levels of hepatic lipase provides new insights into the metabolism of HDL.

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“…VLDL (d Ͻ 1.006 g/ml) were isolated by ultracentrifugation (24) and the HDL fraction was obtained after precipitation of LDL in the infranatant (d Ͼ 1.006 g/ml) with heparin and MnCl 2 (25). The cholesterol content of HDL 2 and HDL 3 subfractions prepared by a precipitation method was also determined (26). Apolipoprotein B concentrations were measured in plasma and infranatant (LDL-apolipoprotein B; d Ͼ 1.006 g/ml) by the rocket immunoelectrophoretic method of Laurell (23), as previously described (27).…”

Section: Study Sample 2 Of Nondiabetic Subjectsmentioning

confidence: 99%

Molecular scanning of the human PPARα gene: association of the L162V mutation with hyperapobetalipoproteinemia

Vohl

Lepage

Gaudet

et al. 2000

Journal of Lipid Research

161

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Peroxisome proliferator-activated receptor alpha (PPAR ␣ ) is a member of the steroid hormone receptor super family involved in the control of cellular lipid utilization. This makes PPAR ␣ a candidate gene for type 2 diabetes and dyslipidemia. The aim of this study was to investigate whether genetic variation in the human PPAR ␣ gene can influence the risk of type 2 diabetes and dyslipidemia among French Canadians. We therefore first determined the genomic structure of human PPAR ␣ , and then designed intronic primers to sequence the coding region and the exon-intron boundaries of the gene in 12 patients with type 2 diabetes and in 2 nondiabetic subjects. Sequence analysis revealed the presence of a L162V missense mutation in exon 5 of one diabetic patient. Leucine 162 is contained within the DNA binding domain of the human PPAR ␣ gene, and is conserved among humans, mice, rats, and guinea pigs. We subsequently screened a sample of 121 patients newly diagnosed with type 2 diabetes and their age and sexmatched nondiabetic controls, recruited from the Saguenay-Lac-St-Jean region of Northeastern Quebec, for the presence of the L162V mutation by a PCR-RFLP based method. There was no difference in L162 homozygote or V162 carrier frequencies between diabetics and nondiabetics. However, whether diabetic or not, carriers of the V162 allele had higher plasma apolipoprotein B levels compared to noncarriers ( P ‫؍‬ 0.05). To further this association, we screened another sample of 193 nondiabetic subjects recruited in the greater Quebec City area. Carriers of the V162 allele compared with homozygotes of the L162 allele had significantly higher concentrations of plasma total and LDL-apolipoprotein B as well as LDL cholesterol ( P р 0.02). These results suggest an association between the PPAR ␣ V162 allele and the atherogenic/hyperapolipoprotein B dyslipidemia.

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Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure

Cited by 711 publications

References 48 publications

Lipid and lipoprotein levels in premenopausal systemic lupus erythematosus patients

Lipid and lipoprotein levels in premenopausal systemic lupus erythematosus patients

Low levels of high density lipoproteins in Turks, a population with elevated hepatic lipase: high density lipoprotein characterization and gender-specific effects of apolipoprotein E genotype

Molecular scanning of the human PPARα gene: association of the L162V mutation with hyperapobetalipoproteinemia

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