Lipids and lipoproteins as coronary risk factors in non-insulin-dependent diabetes mellitus

Syvänne, Mikko; Taskinen, Marja‐Riitta

doi:10.1016/s0140-6736(97)90024-6

Cited by 209 publications

(139 citation statements)

References 31 publications

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“…The recognition that the postprandial state is a cluster of metabolic abnormalities could open new targets for therapies aiming to prevent cardiovascular complications [76]. Postprandial lipemia (fat intolerance) is a distinct component of diabetic dyslipidaemia [7,8,77,78]. Several studies have shown that the response of plasma triglycerides to a standard fat load is much greater in Type 2 diabetic subjects than in non-diabetic subjects matched for age, sex and BMI [7,8,77,78,79].…”

Section: Fat Intolerance In Type 2 Diabetesmentioning

confidence: 99%

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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: Fat Intolerance In Type 2 Diabetesmentioning

confidence: 99%

“…Recent developments have recognized the complex nature of diabetic dyslipidaemia that is a cluster of potentially atherogenic lipid and lipoprotein abnormalities [7]. Two core components of diabetic dyslipidaemia are increased plasma triglycerides and low concentrations of HDL cholesterol.…”

mentioning

confidence: 99%

Diabetic dyslipidaemia: from basic research to clinical practice*

2003

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“…large, less dense VLDL) or less cardioprotective (i.e. small, dense HDL) (Freedman et al, 1998); also these dyslipidemic features are part of the lipoprotein subclass profile in type II diabetes (Syvänne and Taskinen, 1997). It is therefore important to investigate effects of n-3 FA on subclasses and size of lipoproteins in subjects with type II diabetes (Syvänne and Taskinen, 1997;Julius, 2003;Steinmetz, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…small, dense HDL) (Freedman et al, 1998); also these dyslipidemic features are part of the lipoprotein subclass profile in type II diabetes (Syvänne and Taskinen, 1997). It is therefore important to investigate effects of n-3 FA on subclasses and size of lipoproteins in subjects with type II diabetes (Syvänne and Taskinen, 1997;Julius, 2003;Steinmetz, 2003). However, such investigations in diabetes by standard methods (ultracentrifugation, gradient gel electrophoresis) have so far given sparse and diverging results (Luo et al, 1998;Patti et al, 1999;Petersen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Effects of marine n-3 fatty acid supplementation on lipoprotein subclasses measured by nuclear magnetic resonance in subjects with type II diabetes

et al. 2007

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Objective: To measure effects of fish oil supplements on lipoprotein subclasses by nuclear magnetic resonance (NMR) in subjects with type II diabetes and relate them to insulin sensitivity. Design: Two-armed, parallel, placebo-controlled, randomized. Subjects: Normotriglyceridemic subjects with type II diabetes without insulin treatment were given either fish oil (n ¼ 12, median intake 5.9 g/day total n-3 fatty acids (FA) (1.8 g 20:5n-3, 3.0 g 22:6n-3)) or corn oil (n ¼ 14, 8.5 g/day 18:2n-6 FA). Methods: Size and concentration of lipoproteins subclasses were measured by NMR, insulin sensitivity by hyperinsulinemic, isoglycemic clamps. Results: After 9 weeks, there were differences between those treated with fish and corn oil with respect to very low-density lipoprotein (VLDL) size (median À15 vs þ 0.6%, P ¼ 0.001), particle concentrations of large VLDL (À99 vs À4.1%, P ¼ 0.041) and small high-density lipoprotein (HDL) (À12 vs þ 10%, P ¼ 0.051). Compared with corn oil fish oil tended to increase HDL size and small low-density lipoprotein ( LDL) concentration (P ¼ 0.063 and 0.068, respectively, for differences between groups). There was no effect on oxidized LDL. Insulin sensitivity (glucose utilization) decreased in the fish oil group compared with the corn oil group (P ¼ 0.049). The decrease in insulin sensitivity did not correlate with the effects on lipoprotein subclasses. Conclusions: A high intake of n-3 FA exerts effects on several lipoprotein subclasses without obvious influence from changes in insulin sensitivity.

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“…9 Hypertriglyceridemia, low HDL (high-density lipoprotein) and small dense LDL particles are common lipid abnormalities in individuals with insulin resistance and type 2 diabetes mellitus. 10 In healthy volunteers, partly oxidized LDL concentrations are correlated with insulin resistance and its metabolic consequences. 11 Susceptibility of LDL to oxidation has also been associated with increasing levels of total and abdominal adiposity.…”

Section: Introductionmentioning

confidence: 99%

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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Lipids and lipoproteins as coronary risk factors in non-insulin-dependent diabetes mellitus

Cited by 209 publications

References 31 publications

Diabetic dyslipidaemia: from basic research to clinical practice*

Diabetic dyslipidaemia: from basic research to clinical practice*

Effects of marine n-3 fatty acid supplementation on lipoprotein subclasses measured by nuclear magnetic resonance in subjects with type II diabetes

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

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