Literature DB >> 10645915

Accumulation of apolipoprotein C-I-rich and cholesterol-rich VLDL remnants during exaggerated postprandial triglyceridemia in normolipidemic patients with coronary artery disease.

J Björkegren1, S Boquist, A Samnegârd, P Lundman, P Tornvall, C G Ericsson, A Hamsten.   

Abstract

BACKGROUND: Exaggerated postprandial triglyceridemia is common in normolipidemic patients with coronary artery disease (CAD). Alterations in the composition of triglyceride-rich lipoproteins (TRLs) are likely to underlie this metabolic disturbance. However, the composition of very-low-density lipoproteins (VLDLs), which are the most abundant postprandial TRLs, has never been defined in CAD patients. METHODS AND
RESULTS: We examined postprandial changes in the number and composition of VLDLs in middle-aged, normolipidemic CAD patients and control subjects. TRLs from 14 patients and 14 control subjects aged 45 to 55 years were subfractionated by density gradient ultracentrifugation into Svedberg flotation rate (Sf) fractions >400, 60 to 400, and 20 to 60. The VLDLs were separated from chylomicron remnants by immunoaffinity chromatography. In CAD patients, the postprandial concentrations of triglycerides and large (Sf 60 to 400) VLDL particles were elevated. In addition, their postprandial large VLDLs were enriched in apolipoprotein (apo) C-I and their postprandial small (Sf 20 to 60) VLDL remnants were enriched with apo C-I and cholesterol.
CONCLUSIONS: Perturbed handling of postprandial triglycerides in normolipidemic CAD patients involves the accumulation of apo C-I-rich large VLDL particles and the generation of small, apo C-I- and cholesterol-rich VLDL remnants.

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Year:  2000        PMID: 10645915     DOI: 10.1161/01.cir.101.3.227

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  9 in total

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2.  Constitutive inhibition of plasma CETP by apolipoprotein C1 is blunted in dyslipidemic patients with coronary artery disease.

Authors:  Xavier Pillois; Thomas Gautier; Benjamin Bouillet; Jean-Paul Pais de Barros; Aline Jeannin; Bruno Vergès; Jacques Bonnet; Laurent Lagrost
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3.  The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat.

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4.  Pitavastatin prevents postprandial endothelial dysfunction via reduction of the serum triglyceride level in obese male subjects.

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Review 5.  Clinical considerations and mechanistic determinants of postprandial lipemia in older adults.

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6.  Apolipoprotein CI is a physiological regulator of cholesteryl ester transfer protein activity in human plasma but not in rabbit plasma.

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7.  DHA attenuates postprandial hyperlipidemia via activating PPARα in intestinal epithelial cells.

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8.  The apolipoprotein C-I content of very-low-density lipoproteins is associated with fasting triglycerides, postprandial lipemia, and carotid atherosclerosis.

Authors:  John-Bjarne Hansen; José A Fernández; Ann-Trude With Notø; Hiroshi Deguchi; Johan Björkegren; Ellisiv B Mathiesen
Journal:  J Lipids       Date:  2011-07-06

9.  The ApoC-I content of VLDL particles is associated with plaque size in persons with carotid atherosclerosis.

Authors:  Ann-Trude With Notø; Ellisiv Bøgeberg Mathiesen; Jan Brox; Johan Björkegren; John-Bjarne Hansen
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  9 in total

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