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

BioMed Research International
Lei FengJiasui Huang

Abstract

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.

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Citations

Mar 7, 2020·Journal of Zhejiang University. Science. B·Zhi-Feng ZhouJin-Lei Lv
Apr 3, 2019·International Journal of Molecular Sciences·Yen-Chung LinChiung-Chi Peng
Nov 6, 2018·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·Yanjuan HouLihua Wang
May 18, 2021·World Journal of Diabetes·Alla MitrofanovaAlessia Fornoni

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Methods Mentioned

BETA
transfections
PCR
light microscopy

Software Mentioned

SPSS
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