Selenium deficiency-induced redox imbalance leads to metabolic reprogramming and inflammation in the liver

文献类型： 外文期刊

第一作者： Tang, Chaohua

作者： Tang, Chaohua;Li, Shuang;Zhang, Kai;Li, Jing;Han, Yunsheng;Zhan, Tengfei;Zhao, Qingyu;Guo, Xiaoqing;Zhang, Junmin;Tang, Chaohua;Li, Shuang;Zhang, Kai;Li, Jing;Han, Yunsheng;Zhan, Tengfei;Zhao, Qingyu;Guo, Xiaoqing;Zhang, Junmin

作者机构：

关键词： Selenium deficiency; Redox imbalance; Metabolic reprogramming; Inflammation; Pig liver

期刊名称：REDOX BIOLOGY （ 影响因子：11.799； 五年影响因子：12.038 ）

ISSN： 2213-2317

年卷期： 2020 年 36 卷

页码：

收录情况： SCI

摘要： Selenium (Se) intake disequilibrium is associated with many human diseases (e.g., Keshan disease and type 2 diabetes). To understand the mechanism of Se deficiency-induced hepatic pathogenesis, a pure line pig model was established by feeding a diet with either 0.07 mg/kg Se or 0.3 mg/kg Se for 16 weeks. The hepatic metabolome, lipidome, global proteome, and whole transcriptome were analyzed. Se deficiency causes a redox imbalance via regulation of selenoproteins at both the mRNA and protein level, and blocks the glutathione antioxidant system along with enhanced glutathione synthesis and catabolism. The Warburg effect was observed by enhanced activation of the glycolysis and phosphate pentose pathways. The tricarboxylic acid cycle was dysfunctional since the preliminary metabolites decreased and shifted from using glycolysis origin substrates to a glutamine catabolism-preferred metabolic mode. The reprogrammed central carbon metabolism induced widely restrained lipid synthesis. In addition, a Se deficiency initiated inflammation by activating the NF-kappa B pathway through multiple mechanisms. These results identified the potential metabolic vulnerability of the liver in response to a Se deficiency-induced redox imbalance and possible therapeutic or intervention targets.

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