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Diet and Cardiovascular Health: Chylomicron Remnants and Their Emerging Roles in Vascular Dysfunction in Atherogenesis

Chylomicron and apoB48 metabolism in the JCR:LA corpulent rat, a model for the metabolic syndrome

R. Mangat, J. Su, P.G. Scott, J.C. Russell, D.F. Vine, S.D. Proctor
Biochemical Society Transactions May 22, 2007, 35 (3) 477-481; DOI: 10.1042/BST0350477
R. Mangat
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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J. Su
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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P.G. Scott
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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J.C. Russell
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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D.F. Vine
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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S.D. Proctor
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada, T6G 2PS
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  • For correspondence: spencer.proctor@ualberta.ca
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Abstract

Postprandial (PP) lipaemia is a significant contributor to the development of dyslipidaemia and cardiovascular disease (CVD). It is also evident that PP lipaemia is prevalent during conditions of obesity and insulin resistance (IR) and may contribute to increased progression of CVD. Our group has assessed the potential of the obese JCR:LA-cp rat as a model of PP lipaemia in order to explore CM (chylomicron) metabolism during the onset and development of IR in the metabolic syndrome. Studies confirm that both fasting plasma and PP apoB48 (apolipoprotein B48) area under the curve are significantly elevated in the obese JCR:LA-cp phenotype as compared with lean controls. Mechanistic studies have also shown that the concentration of lymphatic CM apoB48 and CM size are significantly increased in this model. Furthermore, PP dyslipidaemia in the obese rat can be improved acutely with supplementation of n−3 polyunsaturated fatty acids. Using a different approach, we have subsequently hypothesized that the vascular remodelling that accompanies IR may explain accelerated entrapment of apoB48-containing particles. Small leucine-rich proteoglycans (including biglycan and decorin) have been observed to co-localize with apoB in human tissue. However, the potential impact of IR on vascular remodelling, particularly in the presence of obesity, remains unclear. Preliminary observations from the JCR:LA-cp model indicate that biglycan protein core content increases with age and is exacerbated by IR, suggestive of pro-atherogenic remodelling. The focus of this review is to contribute to the perspective of PP lipaemia in CVD risk associated with the metabolic syndrome through the use of animal models.

  • animal model
  • arterial proteoglycan
  • atherosclerosis
  • chylomicron remnant
  • insulin resistance
  • obesity
  • postprandial lipaemia

Footnotes

  • Diet and Cardiovascular Health: Chylomicron Remnants and Their Emerging Roles in Vascular Dysfunction in Atherogenesis: Biochemical Society Focused Meeting held at The Royal Veterinary College, London, U.K., 18–19 December 2006. Organized and Edited by K. Botham and C. Wheeler-Jones (Royal Veterinary College, London, U.K.).

Abbreviations: apo, apolipoprotein; CVD, cardiovascular disease; CM, chylomicron; CMR, CM remnant; ERK, extracellular-signal-regulated kinase; IR, insulin resistance; LDL, low-density lipoprotein; LPL, lipoprotein lipase; PCSK-9, proprotein convertase subtilisin kexin type 9; PUFA, polyunsaturated fatty acid; PP, postprandial; SREBP, sterol regulatory element-binding protein; TAG, triacylglycerol; TGF, transforming growth factor; VLDL, very-low-density lipoprotein

  • © 2007 Biochemical Society
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June 2007

Volume: 35 Issue: 3

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Chylomicron and apoB48 metabolism in the JCR:LA corpulent rat, a model for the metabolic syndrome
R. Mangat, J. Su, P.G. Scott, J.C. Russell, D.F. Vine, S.D. Proctor
Biochemical Society Transactions Jun 2007, 35 (3) 477-481; DOI: 10.1042/BST0350477
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Chylomicron and apoB48 metabolism in the JCR:LA corpulent rat, a model for the metabolic syndrome
R. Mangat, J. Su, P.G. Scott, J.C. Russell, D.F. Vine, S.D. Proctor
Biochemical Society Transactions Jun 2007, 35 (3) 477-481; DOI: 10.1042/BST0350477

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  • Article
    • Abstract
    • Introduction to the clinical problem
    • JCR:LA-cp rat as a model of PP lipaemia
    • Hypertriglyceridaemia and VLDL overproduction: a major feature of IR
    • The role of insulin in intestinal CM production and metabolism
    • Effect of n−3 PUFA (polyunsaturated fatty acid) supplementation on PP lipaemia in the JCR:LA-cp rat
    • CMRs: increased atherogenicity for the metabolic syndrome
    • Conclusion
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Keywords

animal model
arterial proteoglycan
atherosclerosis
chylomicron remnant
insulin resistance
obesity
postprandial lipaemia

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