Selenite exacerbates hepatic insulin resistance in mouse model of type 2 diabetes through oxidative stress-mediated JNK pathway
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- 作者：Jun Zhou ; hustzhj@hust.edu.cn" class="auth_mail" title="E-mail the corresponding author ; Gang Xu ; Zhaoshuai Bai ; Kaicheng Li ; Junyan Yan ; Fen Li ; Shuai Ma ; Huibi Xu ; Kaixun Huang ; hxxzrf@hust.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：ANOVA ; analysis of variance ; ASK1 ; apoptosis signal-regulated kinase 1 ; AUC ; area under the curve ; BSA ; bovine serum albumin ; ECL ; enhanced chemiluminescence ; FBG ; fasting blood glucose ; FPI ; fasting plasma insulin ; G6Pase ; glucose 6-phosphatase ; GK ; glucokinase ; GPx ; glutathione peroxidase ; GTT ; glucose tolerance test ; HFD ; high-fat diet ; HOMA-IR ; homeostatic model assessment of insulin resistance ; IR ; insulin receptor ; IRS ; insulin receptor substrate ; ITT ; insulin tolerance test ; JNK ; c-Jun. N
- 刊名：Toxicology and Applied Pharmacology
- 出版年：2015
- 出版时间：15 December 2015
- 年：2015
- 卷：289
- 期：3
- 页码：409-418
- 全文大小：966 K
文摘
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Selenite exacerbates hepatic insulin resistance in HFD/STZ-induced diabetic mice.
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Selenite elevates hepatic gluconeogenesis and reduces glycolysis in diabetic mice.
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Selenite exacerbates hepatic oxidative stress and triggers JNK signaling pathway.
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Selenite elevates hepatic selenoprotein P expression in diabetic mice.