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BioMed Research International
Volume 2018, Article ID 5045182, 10 pages
https://doi.org/10.1155/2018/5045182
Research Article

Vildagliptin Can Alleviate Endoplasmic Reticulum Stress in the Liver Induced by a High Fat Diet

Xiaoqing Ma,1,2,3,4 Wenhua Du,1,2,3,5 Shanshan Shao,1,2,3 Chunxiao Yu,1,2,3 Lingyan Zhou,6 and Fei Jing1,2,3

1Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China
2Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong 250021, China
3Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Jinan, Shandong 250021, China
4Department of Endocrinology, Jining No. 1 People’s Hospital, No. 6 Health Road, Rencheng, Jining 272011, China
5Department of Endocrinology, Linyi People’s Hospital, Linyi, Shandong 276001, China
6Department of Endocrinology, The Second Hospital of Shandong University, No. 247 Beiyuan Street, Jinan 250033, China

Correspondence should be addressed to Fei Jing; moc.361@5170iefgnij

Received 4 September 2017; Accepted 13 December 2017; Published 12 March 2018

Academic Editor: Kusum Kharbanda

Copyright © 2018 Xiaoqing Ma 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

Purpose. We investigated whether a DDP-4 inhibitor, vildagliptin, alleviated ER stress induced by a high fat diet and improved hepatic lipid deposition. Methods. C57BL/6 mice received standard chow diet (CD), high fat diet (HFD), and HFD administered with vildagliptin (50 mg/Kg) (V-HFD). After administration for 12 weeks, serum alanine aminotransferase, glucose, cholesterol, triglyceride, and insulin levels were analyzed. Samples of liver underwent histological examination and transmission electron microscopy, real-time PCR for gene expression levels, and western blots for protein expression levels. ER stress was induced in HepG2 cells with palmitic acid and the effects of vildagliptin were investigated. Results. HFD mice showed increased liver weight/body weight (20.27%) and liver triglycerides (314.75%) compared to CD mice, but these decreased by 9.27% and 21.83%, respectively, in V-HFD mice. In the liver, HFD induced the expression of ER stress indicators significantly, which were obviously decreased by vildagliptin. In vitro, the expressions of molecular indicators of ER stress were reduced in HepG2 when vildagliptin was administered. Conclusions. Vildagliptin alleviates hepatic ER stress in a mouse high fat diet model. In HepG2 cells, vildagliptin directly reduced ER stress. Therefore, vildagliptin may be a potential agent for nonalcoholic fatty liver disease.