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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
06:47

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

Published on: January 28, 2021

Lipoprotein lipase deficiency in chronic kidney disease is accompanied by down-regulation of endothelial GPIHBP1

Nosratola D Vaziri1, Jun Yuan, Zhenmin Ni

  • 1Division of Nephrology and Hypertension, University of California, Irvine, Irvine, CA, USA. ndvaziri@uci.edu

Clinical and Experimental Nephrology
|October 20, 2011
PubMed

Insights

Chronic kidney disease (CKD) reduces both lipoprotein lipase (LPL) and GPIHBP1 expression, leading to hypertriglyceridemia. This study reveals a dual deficiency contributing to impaired lipid metabolism and associated health issues in CKD.

Area of Science:

  • Biochemistry
  • Renal Physiology
  • Lipid Metabolism

Background:

  • Chronic renal failure (CRF) is linked to hypertriglyceridemia due to impaired very low density lipoprotein (VLDL) and chylomicron clearance, often caused by lipoprotein lipase (LPL) dysfunction.
  • Glycosylphosphatidylinositol-anchored binding protein 1 (GPIHBP1) is crucial for anchoring LPL to the endothelium and managing LPL activity.
  • Deficiency in GPIHBP1 leads to severe hypertriglyceridemia and reduced LPL activity, highlighting its regulatory role.

Purpose of the Study:

  • To investigate the impact of chronic kidney disease (CKD) on the expression of GPIHBP1.
  • To understand the relationship between CKD, LPL deficiency, and GPIHBP1 expression.

Main Methods:

  • Expression levels of GPIHBP1 and LPL were assessed using reverse transcriptase-polymerase chain reaction, Western blot, and immunohistochemical analyses.
  • These analyses were performed on adipose tissue, skeletal muscle, and myocardium of rats subjected to 5/6 nephrectomy (CRF) or sham-operation (control).

Main Results:

  • CRF rats exhibited severe hypertriglyceridemia compared to controls.
  • A significant reduction in LPL mRNA and protein was observed in the skeletal muscle, myocardium, and adipose tissue of CRF rats.
  • Parallel reductions in GPIHBP1 mRNA abundance and immunostaining were found in the same tissues of CRF rats.

Conclusions:

  • Lipoprotein lipase (LPL) deficiency in chronic kidney disease (CKD) is exacerbated by a concurrent deficiency in GPIHBP1.
  • These combined deficiencies impair the clearance of triglyceride-rich lipoproteins.
  • The resulting hypertriglyceridemia, diminished lipid availability, and other complications like cachexia and atherosclerosis are linked to these molecular defects.
Abstract

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