Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size

Tribble, Diane L.; Holl, Laura Glines; Wood, Peter D.; Krauss, Ronald M.

doi:10.1016/0021-9150(92)90255-f

Cited by 455 publications

(199 citation statements)

References 28 publications

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“…The retained LDL particles in the intima are exposed to modification under conditions of oxidative stress. Small dense LDL shows an increased susceptibility to oxidation and glycation of LDL further aggravating this susceptibility to oxidation [132,133,134,135]. A debated question is whether the size of LDL or its integral physical properties determine LDL oxidisability.…”

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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Section: Why Is Small Dense Ldl Highly Atherogenic?mentioning

confidence: 99%

Diabetic dyslipidaemia: from basic research to clinical practice*

2003

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“…Diabetic patients may be particularly vulnerable in this regard, given the increased oxidative stress associated with this disease (Giugliano et al, 1996). One hypothesis for the accelerated atherosclerosis in diabetes is related to the increased oxidative vulnerability of glycosylated LDL (Lyons & Jenkins, 1997) and small, dense LDL particles (Tribble et al, 1992). If fish oil supplementation further impairs the oxidation resistance of LDL, this might lead to accelerated atherogenesis in diabetic patients.…”

Section: Introductionmentioning

confidence: 99%

Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes

Pedersen¹,

Petersen²,

Major‐Pedersen

et al. 2003

Eur J Clin Nutr

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“…Smaller, denser LDL particles are associated with increased risk of coronary heart disease (CHD) 1 because they are more susceptible to oxidative modification, 2 an initial step in the atherosclerotic process. We have previously demonstrated that plasma LDL concentrations increased and the size of LDL particles decreased after menopause, whether naturally or surgically induced.…”

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confidence: 99%

Different Effects of Oral Conjugated Equine Estrogen and Transdermal Estrogen Replacement Therapy on Size and Oxidative Susceptibility of Low-Density Lipoprotein Particles in Postmenopausal Women

et al. 2002

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Background-Postmenopausal estrogen replacement therapy (ERT) has an antioxidant effect that opposes the oxidation of LDL particles. Oral ERT-induced increases in plasma triglyceride, however, decrease LDL particle size, which may counteract this antioxidant effect. Because transdermal ERT decreases plasma triglyceride, it may not decrease LDL particle size and may preserve estrogen's antioxidant effect. The present study investigates whether transdermal ERT can eliminate the adverse effects of oral ERT on the size and oxidative susceptibility of LDL in postmenopausal women. Methods and Results-Postmenopausal women received no treatment (nϭ12) or were treated with either 0.625 mg oral conjugated equine estrogen daily (nϭ16) or with transdermal estradiol (50 g/d, nϭ16) for 3 months. Plasma lipids and the diameter of LDL particles were determined. Susceptibility of LDL to oxidation was analyzed by incubation with CuSO 4 and subsequent measurement of thiobarbituric acid reactive substance (TBARS) concentrations. Oral ERT significantly increased plasma triglyceride and decreased LDL diameter but did not affect LDL-derived TBARS concentrations. In contrast, transdermal ERT significantly decreased the concentrations of plasma triglyceride and LDL-derived TBARS and significantly increased LDL diameter. Estrogen-induced changes in LDL diameter correlated negatively with changes in plasma triglyceride (rϭϪ0.51, PϽ0.001) and LDL-derived TBARS (rϭϪ0.50, PϽ0.001). Conclusions-Because transdermal, but not oral ERT, decreases plasma triglyceride and produces larger LDL particles that are resistant to oxidation, the antioxidant effect of estrogen can be preserved.

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Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size

Cited by 455 publications

References 28 publications

Diabetic dyslipidaemia: from basic research to clinical practice*

Diabetic dyslipidaemia: from basic research to clinical practice*

Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes

Different Effects of Oral Conjugated Equine Estrogen and Transdermal Estrogen Replacement Therapy on Size and Oxidative Susceptibility of Low-Density Lipoprotein Particles in Postmenopausal Women

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