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BioMed Research International
Volume 2017, Article ID 1414070, 10 pages
Research Article

High Glucose Promotes CD36 Expression by Upregulating Peroxisome Proliferator-Activated Receptor γ Levels to Exacerbate Lipid Deposition in Renal Tubular Cells

1Graduate School, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
2Hospital Infection Control Department, The Suining Central Hospital, Suining 629000, China

Correspondence should be addressed to Lei Feng; moc.361@228ielgnef

Received 20 January 2017; Revised 19 March 2017; Accepted 2 April 2017; Published 12 April 2017

Academic Editor: Koichiro Wada

Copyright © 2017 Lei Feng 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.


Diabetic kidney disease (DKD) appears to be closely related to lipid deposition in kidney. The aim of this study was to determine whether high glucose (HG) exacerbated lipid deposition by increasing CD36 expression via AKT-PPARγ signaling pathway. Our results showed that HG activated AKT signaling pathway, followed by an increase in PPARγ that induced CD36 overexpression, ultimately causing lipid deposition in HK-2 cells. We also found that inhibition of AKT-PPARγ signaling pathway or knockdown of CD36 could reduce HG-induced lipid accumulation in HK-2 cells. These results indicated that AKT-PPARγ signaling pathway mediated HG-induced lipid deposition by upregulating CD36 expression in HK-2 cells and that inhibition of AKT-PPARγ signaling pathway had the potential beneficial effects of reducing lipid deposition in diabetic kidney.