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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 9032792, 14 pages
https://doi.org/10.1155/2017/9032792
Research Article

Green Tea Polyphenols Ameliorate the Early Renal Damage Induced by a High-Fat Diet via Ketogenesis/SIRT3 Pathway

1Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
3Department of Nutrition and Food Hygiene, School of Public Health and Management, Binzhou Medical University, Yantai 264003, China
4Department of Hotel Management, Tourism University, Guilin 541000, China
5Department of Nutrition and Food Hygiene, Xinxiang Medical University, Xinxiang 453000, China
6Kecheng People’s Hospital, Quzhou 324000, China
7School of Nursing, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
8Department of Clinical Nutrition, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China

Correspondence should be addressed to Xuezhi Zuo; nc.ude.umjt.hjt@7691ouZ and Chenjiang Ying; nc.ude.tsuh@jcgniy

Received 28 March 2017; Revised 12 May 2017; Accepted 25 May 2017; Published 26 July 2017

Academic Editor: Giuseppe Grosso

Copyright © 2017 Weijie Yi 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.

Abstract

Scope. Several reports in the literature have suggested the renoprotective effects of ketone bodies and green tea polyphenols (GTPs). Our previous study found that GTP consumption could elevate the renal expression of the ketogenic rate-limiting enzyme, which was decreased by a high-fat diet (HFD) in rats. Here, we investigated whether ketogenesis can mediate renoprotection by GTPs against an HFD. Methods and Results. Wistar rats were fed a standard or HFD with or without GTPs for 18 weeks. The renal oxidative stress level, kidney function, renal expression, and activity levels of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2) and sirtuin 3(SIRT3) were detected. The increased renal oxidative stress and the loss of renal function induced by the HFD were ameliorated by GTPs. Renal ketogenesis and SIRT3 expression and activity levels, which were reduced by the HFD, were restored by GTPs. In vitro, HEK293 cells were transfected with the eukaryotic expression plasmid pcDNA HMGCS2. GTP treatment could upregulate HMGCS2 and SIRT3 expression. Although SIRT3 expression was not affected by HMGCS2 transfection, the 4-hydroxy-2-nonenal (4-HNE) level and the acetyl-MnSOD (K122)/MnSOD ratio were reduced in HMGCS2-transfected cells in the context of H2O2. Conclusion. The ketogenesis/SIRT3 pathway mediates the renoprotection of GTPs against the oxidative stress induced by an HFD.