Comparison of Various Electrophoretic Characteristics of LDL Particles and Their Relationship to the Risk of Ischemic Heart Disease

St‐Pierre, Annie; Ruel, Isabelle L.; Cantin, Bernard; Dagenais, Gilles R.; Bernard, Paul‐Marie; Després, Jean‐Pierre; Lamarche, Benoı̂t

doi:10.1161/hc4401.098490

Cited by 236 publications

(168 citation statements)

References 19 publications

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“…Intra-and interassay coefficients of variation for this measurement were both p6.0%, as described previously (Couillard et al, 2003). Distinct subpopulations of LDL particles in whole plasma were separated by size using a nondenaturing 2-16% gradient gel electrophoresis, as described previously (St Pierre et al, 2001;Archer et al, 2003b). Postheparin (60 IU/kg body weight) lipoprotein lipase (LPL) and hepatic lipase (HL) activities were measured after preincubation with sodium dodecyl sulfate (SDS), as previously described (Watson et al, 1995;Bower et al, 2002).…”

Section: Laboratory Methodsmentioning

confidence: 99%

Kinetics of plasma apolipoprotein C-III as a determinant of diet-induced changes in plasma triglyceride levels

Desroches

Deshaies

et al. 2007

Eur J Clin Nutr

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Objective: To compare the effect of a high monounsaturated fatty acid (MUFA) diet and of a control low-fat diet consumed under ad libitum conditions on plasma apolipoprotein (apo) C-III metabolism. Design: Randomized, two-arm parallel dietary trial. Setting: Diets were prepared and consumed at the metabolic kitchen of the Department of Food Sciences and Nutrition, and laboratory analyses were performed at the Institute of Nutraceuticals and Functional Foods at Laval University. Subjects and interventions: Eighteen men were randomly assigned to either the high MUFA diet or the low-fat control diet, which they consumed for 6-7 weeks. Before and after the dietary intervention, subjects received a primed-constant infusion of [5,5,5-D 3 ]-L-leucine for 12 h under constant feeding conditions for the determination of plasma apoC-III kinetics. Results: The high-MUFA diet and the low-fat control diet had no significant impact on plasma apoC-III production rate (PR) or fractional catabolic rate. However, diet-induced variations in plasma apoCIII PR predicted the reduction in plasma triglycerides and apoC-III levels (r ¼ 0.85, Po0.01 and r ¼ 0.73, Po0.05, respectively) in the high MUFA group only. Conclusions: These results suggest that the hypotriglyceridemic effect of a high-MUFA diet may be attributable in part to a reduced hepatic production of apoC-III.

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Section: Laboratory Methodsmentioning

confidence: 99%

Kinetics of plasma apolipoprotein C-III as a determinant of diet-induced changes in plasma triglyceride levels

Desroches

Deshaies

et al. 2007

Eur J Clin Nutr

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“…Both LDL size and the number of particles seems to increase synergistically the risk of CHD [120,121]. Recently convincing tenets seem to explain the atherogeneity of small dense LDL particles.…”

Section: Why Is Small Dense Ldl Highly Atherogenic?mentioning

confidence: 99%

Diabetic dyslipidaemia: from basic research to clinical practice*

2003

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The recognition that the increase of plasma triglyceride rich lipoproteins (TRLs) is associated with multiple alterations of other lipoproteins species that are potentially atherogenic has expanded the picture of diabetic dyslipidaemia. The discovery of heterogeneity within major lipoprotein classes VLDL, LDL and HDL opened new avenues to reveal the specific pertubations of diabetic dyslipidaemia. The increase of large VLDL 1 particles in Type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense LDL and small dense HDL particles. Together these components comprise the atherogenic lipid triad. Notably the malignant nature of diabetic dyslipidaemia is not completely shown by the lipid measures used in clinical practice. The key question is what are the mechanisms behind the increase of VLDL 1 particles in diabetic dyslipidaemia? Despite the advances of recent years, our understanding of VLDL assembly and secretion is still surprisingly incomplete. To date it is still unclear how the liver is able to regulate the amount of triglycerides incorporated into VLDL particles to produce either VLDL 1 or VLDL 2 particles. The current evidence suggests that the machinery driving VLDL assembly in the liver includes (i) low insulin signalling via PI-3 kinase pathway that enhances lipid accumulation into "nascent" VLDL particles (ii) up-regulation of SREBP-1C that stimulates de novo lipogenesis and (iii) excess availability of "polar molecules" in hepatocytes that stabilizes apo B 100. Recent data suggest that all these steps could be fundamentally altered in Type 2 diabetes explaining the overproduction of VLDL apo B as well as the ability of insulin to suppress VLDL 1 apo B production in Type 2 diabetes.Recent discoveries have established the transcription factors including PPARs, SREBP-1 and LXRs as the key regulators of lipid assembly in the liver. These observations suggest these factors as a new target to tailor more efficient drugs to treat diabetic dyslipidaemia. [Diabetologia (2003) 46:733-749]

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“…19 Distinct subpopulations of LDL particles were separated in whole plasma using nondenaturating 2-16% gradient gel electrophoresis as previously described. 1 Lowdensity lipoprotein peak particle diameter was identified as the most important subclass of LDL in each individual and was calculated from calibration curves using plasma standards of known diameter. The CV of the calculated particle diameters was estimated to be o1%.…”

Section: Laboratory Methodsmentioning

confidence: 99%

“…A similar approach was used to assess the relative proportion of LDL particles with a diameter 4260 Å (LDL% 4260 Å ) and absolute concentrations of cholesterol in particles with a diameter 4260 Å (LDL-C 4260 Å ). 1 Oxidized LDL (OxLDL) concentrations were measured using a commercial ELISA according to the manufacturer's instructions (Alpco Diagnostics, Windham, NH). C-reactive protein levels were measured with a highly sensitive commercial immunoassay (Dade Behring, Mississauga, ON, Canada) as described previously.…”

Section: Laboratory Methodsmentioning

confidence: 99%

“…1 Recent research on the lipid composition, charge and susceptibility of LDL to oxidation has led to a better understanding of their role in the etiology of atherosclerosis. The phospholipid-depleted surface monolayer of small dense LDL compared with large LDL particles, is responsible for a change in the conformation of apolipoprotein (apo) B-100, which leads to more exposure of proteoglycan-binding regions.…”

Section: Introductionmentioning

confidence: 99%

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Visceral adipose tissue accumulation, secretory phospholipase A2-IIA and atherogenecity of LDL

et al. 2006

Int J Obes

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Objective: The aim of the present study was to investigate the combined impact of visceral adipose tissue (VAT) and secretory group IIA phospholipase A 2 (sPLA 2 -IIA) concentrations on the atherogenicity of low-density lipoprotein (LDL) particles among men. Subjects: Analyses were conducted in 74 mid-obese healthy men (age: (mean7s.d.) 37.9711.7 years). Methods: Plasma levels of sPLA 2 -IIA were measured with a commercial ELISA and VAT levels were assessed by computed tomography. Distinct subpopulations of LDL particles were characterized from whole plasma using nondenaturating 2-16% gradient gel electrophoresis. Results: Data indicated that plasma sPLA 2 -IIA levels were approximately 29% (P ¼ 0.007) higher among men characterized by a higher accumulation of VAT (4142 vs p142 cm 2 ). Men having high plasma sPLA 2 -IIA levels (X127.2 ng/dl, the median value), were characterized by higher levels of plasma cholesterol (C) and apolipoprotein (apo) B, LDL-C, LDL-apoB, oxidized LDL (OxLDL) and by smaller LDL particles compared to men with sPLA 2 -IIAo127.2 ng/dl. Multiple regression analyses showed that plasma triglycerides and sPLA 2 -IIA levels explained 22.7 and 11.8% of the variance in LDL peak particle size, respectively. Levels of VAT and of sPLA 2 -IIA were the strongest correlates of OxLDL levels explaining, respectively, 15.0 and 5.5% of their variability. Conclusion: Both VAT and sPLA 2 -IIA levels modulate the atherogenecity of LDL by accounting for the reduction in their size and their susceptibility to oxidation.

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Comparison of Various Electrophoretic Characteristics of LDL Particles and Their Relationship to the Risk of Ischemic Heart Disease

Cited by 236 publications

References 19 publications

Kinetics of plasma apolipoprotein C-III as a determinant of diet-induced changes in plasma triglyceride levels

Kinetics of plasma apolipoprotein C-III as a determinant of diet-induced changes in plasma triglyceride levels

Diabetic dyslipidaemia: from basic research to clinical practice*

Visceral adipose tissue accumulation, secretory phospholipase A2-IIA and atherogenecity of LDL

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