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International Journal of Endocrinology
Volume 2015 (2015), Article ID 687938, 11 pages
http://dx.doi.org/10.1155/2015/687938
Research Article

Glycolipid Metabolism Disorder in the Liver of Obese Mice Is Improved by TUDCA via the Restoration of Defective Hepatic Autophagy

1Critical Care Medicine, The First Affiliated Hospital of Medical School of Xi’an Jiaotong University, 277 Yanta West Street, Xi’an, Shaanxi 710061, China
2Key Laboratory of Environment and Genes Related to Diseases, Medical School of Xi’an Jiaotong University, Xi’an, Shaanxi 710061, China
3Center for Translational Medicine, The First Affiliated Hospital of Medical School of Xi’an Jiaotong University, 277 Yanta West Street, Xi’an, Shaanxi 710061, China
4Department of Respiratory, The First Affiliated Hospital of Medical School of Xi’an Jiaotong University, 277 Yanta West Street, Xi’an, Shaanxi 710061, China

Received 30 June 2015; Revised 24 October 2015; Accepted 1 November 2015

Academic Editor: Marco Bugliani

Copyright © 2015 Qinyue Guo 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

Objective. Tauroursodeoxycholic acid (TUDCA) has been considered an important regulator of energy metabolism in obesity. However, the mechanism underlying how TUDCA is involved in insulin resistance is not fully understood. We tested the effects of TUDCA on autophagic dysfunction in obese mice. Material and Methods. 500 mg/kg of TUDCA was injected into obese mice, and metabolic parameters, autophagy markers, and insulin signaling molecular were assessed by Western blotting and real-time PCR. Results. The TUDCA injections in the obese mice resulted in a reduced body weight gain, lower blood glucose, and improved insulin sensitivity compared with obese mice that were injected with vehicle. Meanwhile, TUDCA treatment not only reversed autophagic dysfunction and endoplasmic reticulum stress, but also improved the impaired insulin signaling in the liver of obese mice. Additionally, the same results obtained with TUDCA were evident in obese mice treated with the adenoviral Atg7. Conclusions. We found that TUDCA reversed abnormal autophagy, reduced ER stress, and restored insulin sensitivity in the liver of obese mice and that glycolipid metabolism disorder was also improved via the restoration of defective hepatic autophagy.