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

ABSTRACT: 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 anti-oxidant 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 decre

SUBMITTER: Tang C 

PROVIDER: S-EPMC7287308 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature