Purple sweet potato color attenuates hepatic insulin resistance via blocking oxidative stress and endoplasmic reticulum stress in high-fat-diet-treated mice

被引:104
作者
Zhang, Zi-Feng [1 ]
Lu, Jun [1 ]
Zheng, Yuan-Lin [1 ]
Wu, Dong-Mei [1 ]
Hu, Bin [1 ]
Shan, Qun [1 ]
Cheng, Wei [2 ]
Li, Meng-Qiu [1 ]
Sun, Yuan-Yuan [1 ]
机构
[1] Jiangsu Normal Univ, Sch Life Sci, Key Lab Biotechnol Med Plants Jiangsu Prov, Xuzhou 221116, Jiangsu, Peoples R China
[2] China Univ Min & Technol, Sch Environm & Spatial Informat, Xuzhou 221008, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
PSPC; HFD; Insulin resistance; Oxidative stress; ER stress; NAFLD; D-GALACTOSE; LIVER-DISEASE; ACYLATED ANTHOCYANINS; LIPID-ACCUMULATION; INDUCED APOPTOSIS; MOUSE-LIVER; OBESITY; PATHWAY; PROTEIN; CELLS;
D O I
10.1016/j.jnutbio.2012.07.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has been reported to possess a variety of health-promoting properties. Emerging evidence indicates that PSPC can suppress postprandial hyperglycemia via inhibition of alpha-glucosidases. However, the protective effects of PSPC on hepatic insulin resistance and the precise mechanisms underlying these protective effects have never been investigated. In this study, our data showed that PSPC effectively improved the fasting blood glucose level, glucose and insulin tolerance by suppressing reactive oxygen species (ROS) production and by restoring glutathione (GSH) content and antioxidant enzymes' activities. PSPC further prevented the oxidative-stress-mediated endoplasmic reticulum (ER) stress in the livers of high-fat-diet (HFD)-treated mice. Moreover, PSPC dramatically suppressed the c-Jun-N-terminal kinase 1 and I kappa B kinase beta activation and nuclear factor-kappa B p65 nuclear translocation caused by oxidative and ER stress in the livers of HFD-treated mice. Ultimately, PSPC notably restored the impairment of the insulin receptor substrate-1/phosphoinositide 3 kinase/protein kinase B (Akt) insulin signaling in the livers of HFD-treated mice. In conclusion, our findings indicate that PSPC protected against HFD-induced hepatic insulin resistance via decreasing ROS level and blocking ROS-mediated ER stress. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1008 / 1018
页数:11
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