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Experimental Diabetes Research
Volume 2011, Article ID 851280, 10 pages
Research Article

Effect of Exposure of Human Monocyte-Derived Macrophages to High, versus Normal, Glucose on Subsequent Lipid Accumulation from Glycated and Acetylated Low-Density Lipoproteins

1Free Radical Group, The Heart Research Institute, 7 Eliza Street, Newtown, Sydney, NSW 2042, Australia
2Faculty of Medicine, University of Sydney, Sydney, NSW 2006, Australia
3Gene Regulation Group, The Heart Research Institute, Sydney, NSW 2042, Australia
4School of Medical and Molecular Biosciences, University of Technology, Sydney, NSW 2007, Australia

Received 10 May 2011; Revised 29 June 2011; Accepted 1 July 2011

Academic Editor: Mark A. Yorek

Copyright © 2011 Fatemeh Moheimani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. Here we examined the hypothesis that hyperglycaemia may modulate receptor expression and hence lipid accumulation in macrophages. Human monocytes were matured into macrophages in 30 versus 5 mM glucose and receptor expression and lipid accumulation quantified. High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. SR-BI and CD36 protein levels were decreased. Normo- and hyperglycaemic cells accumulated cholesteryl esters from modified LDL to a greater extent than control LDL, but total and individual cholesteryl ester accumulation was not affected by glucose levels. It is concluded that, whilst macrophage scavenger receptor mRNA and protein levels can be modulated by high glucose, these are not key factors in lipid accumulation by human macrophages under the conditions examined.