LDL particle size in mildly hypertriglyceridemic subjects: no relation to insulin resistance or diabetes

Lahdenperä, Sanni; Sane, Timo; Vuorinen-Markkola, Helena; Knudsen, Petteri; Taskinen, Marja‐Riitta

doi:10.1016/0021-9150(94)05450-w

Cited by 39 publications

(19 citation statements)

References 42 publications

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“…In the QCAHS, even when we used the most sensitive cut point suggested in adults (0.9), the false-negative rate was 14% and the false-positive rate was 22%. Similar to results reported in studies of adults (7,8,25,(55)(56)(57)(58)(59), the fasting plasma TG concentration was the strongest independent correlate (negative) of LDL peak particle size in the present pediatric study. This is consistent with the prevailing model for the generation of small LDL particles, which proposes that increased hepatic production of TG-rich lipoproteins (i.e., VLDL) associated with insulin resistance leads to TG-enriched LDL particles through cholesteryl ester transfer proteinmediated exchange of cholesteryl esters from LDL to VLDL particles and of TG from VLDL to LDL particles.…”

Section: Discussionsupporting

confidence: 90%

“…This appears inconsistent with the known association between IRS and a small LDL size. However, in most adult studies, insulin sensitivity was not independently associated with LDL size, and the effect of insulin resistance on LDL size could be explained by the effect of insulin resistance or hyperinsulinemia on VLDL metabolism (7,8,25,(55)(56)(57)(58)(59). Moreover, plasma insulin concentrations reflect both pancreatic insulin secretion and peripheral insulin resistance.…”

Section: Discussionmentioning

confidence: 98%

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Distribution of LDL Particle Size in a Population-Based Sample of Children and Adolescents and Relationship with Other Cardiovascular Risk Factors

Stan¹,

Lévy²,

Delvin³

et al. 2005

Clinical Chemistry

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Background: Smaller, denser LDL particles are associated with an increased risk for cardiovascular diseases (CVD). In youths, data on the distribution of LDL particle size and on its association with other CVD risk factors are limited. Methods: We determined LDL peak particle size by nondenaturing 2%-16% gradient gel electrophoresis in a representative sample of 2249 youths 9, 13, and 16 years of age who participated in a school-based survey conducted in 1999 in the province of Quebec, Canada. Standardized clinical measurements and fasting plasma lipid, glucose, and insulin concentrations were available. Results: The LDL peak particle size distribution was gaussian. The 5th, 50th (median), and 95th percentiles by age and sex were 255.5-258.6, 262.1-263.2, and 268.1-269.5 Å, respectively. The prevalence of the small, dense LDL phenotype (LDL peak particle size <255 Å) was 10% in participants with insulin resistance syndrome (IRS), in contrast to 1% in those without IRS. In a multiple regression analysis, the association of LDL size with other CVD risk factors [apolipoprotein B, HDLcholesterol (HDL-C), triglyceride (TG), and insulin concentrations, and body mass index] was strongest with TG and HDL-C concentrations: a 1 SD increase in log e -transformed TG concentration was associated with

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 98%

Distribution of LDL Particle Size in a Population-Based Sample of Children and Adolescents and Relationship with Other Cardiovascular Risk Factors

Stan¹,

Lévy²,

Delvin³

et al. 2005

Clinical Chemistry

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“…The decrease in LDL size seems to be greater in women than in men. Small dense LDL correlates with measures of insulin resistance but after controlling for triglycerides and HDL cholesterol, no association prevails between LDL size and insulin sensitivity [107,112,113,114,115]. In agreement several studies have confirmed that the concentration of plasma triglyceride is the single most important determinant of the variability of LDL size explaining nearly 50% of the variation in LDL size [114,115].…”

Section: Is Postprandial Lipidemia a Hazard?mentioning

confidence: 74%

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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“…Although non-insulin-dependent diabetes mellitus (NIDDM) is associated with increased plasma levels of small LDL and smaller LDL peak diameter, whether these associations are independent of plasma triglyceride levels is less clear [183][184][185]. Diabetic dyslipidemia reflects increased hepatic VLDL secretion and impaired VLDL and chylomicron clearance [186].…”

Section: Diabetesmentioning

confidence: 98%