| Accession | PRJCA002073 | ||||||||
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| Title | Selenium deficiency-induced redox imbalance leads to metabolic reprogramming and inflammation in liver | ||||||||
| Relevance | Nutriton and Health | ||||||||
| Data types |
Transcriptome or Gene expression
Raw sequence reads TMT 10-plex proteomics data |
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| Organisms | Sus scrofa | ||||||||
| Description | The interplay of selenium (Se), redox homeostasis, and energy metabolism is related to many human metabolic diseases. To explore the underlying mechanisms of suboptimal Se induced liver diseases, we fed pure line pigs with a Se deficiency diet (0.007 mg/kg) for 16 weeks, studied how hepatic metabolome (hydrophilic and lipophilic), global proteome, and whole-transcriptome response to, and identified molecules and pathways involved in. Se deficiency decreased hair, blood, and hepatic Se contents, decreased blood and hepatic anti-oxidant capacity and increased ROS and pro-inflammatory factors levels, and induced lymphocytes infiltration, stripe-like hyperplasia, and sinus expansion in liver. Se deficiency triggered hepatic oxidative stress by down regulating selenoproteins at genes mRNA and protein levels, hindering glutathione system, along with an enhanced glutathione synthesis and catabolism as substrates were decreased and mRNA expression of enzymes involved in were up-regulated. A Warburg effect was observed, as glycolysis were enhanced and significant amounts of glycolytic metabolites were diverted into phosphate pentose pathway for production of NADPH. The TCA cycle was disfunction as the preliminary metabolites were decreased, while glutamine, malic acid, and fumarate were increased, showing that TCA cycle was shifted to a glutamine catabolism preferred mode, rather than using glycolysis origin substrates. The reprogrammed central carbon metabolism also brought out a widely reduction of lipid synthesis. Also, Se deficiency initiating inflammation by activating NF-κB pathway through multiple mechanisms. These results generated a comprehensive picture of the essential physiological role of Se in liver health, which may provide intervention targets for Se deficiency-induced disease in the future. | ||||||||
| Sample scope | Monoisolate | ||||||||
| Release date | 2020-07-17 | ||||||||
| Grants |
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| Submitter | Chaohua Tang (tangchaohua@caas.cn) | ||||||||
| Organization | Institute of Animal Sciences, Chinese Academy of Agricultural Sciences | ||||||||
| Submission date | 2019-12-26 |