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- W966171646 abstract "Objective Oxidants can contribute to cellular signaling via glutathione-(GSH) adducts, which are reversible post-translational modifications of proteins that alter their function. Glutaredoxin-1 (Glrx) is an enzyme that specifically removes these GSH-adducts and modulates enzyme activity. We aimed to study the physiological role of Glrx and protein GSH-adducts in vivo Methods Whole body Glrx knockout mice (Glrx-/-) were created in a C57BL/6J strain and metabolic alterations were monitored over eight months Results Chow fed Glrx-/- mice developed obesity, hepatic steatosis and hyperlipidemia. The key enzyme in hepatic lipid biosynthesis, fatty acid synthase (FASN), was upregulated by 50% in Glrx-/- mice. Liver-specific adenoviral Glrx reconstitution of Glrx-/- mice down-regulated hepatic FASN and normalized hepatic and plasma lipid levels. The central metabolic regulator sirtuin-1 (SirT1), regulates FASN expression. Here, we found that elevated GSH-adducts on SirT1 in Glrx-/- mice inhibited SirT1 activity leading to increased FASN transcription. Conclusions Our data suggest that Glrx regulates SirT1 activity in vivo through GSH-adducts thereby modulating hepatic and plasma lipids." @default.
- W966171646 created "2016-06-24" @default.
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- W966171646 date "2015-04-01" @default.
- W966171646 modified "2023-09-23" @default.
- W966171646 title "Regulatation of hepatic lipid metabolism by glutaredoxin‐1 and protein glutathione‐adducts" @default.
- W966171646 doi "https://doi.org/10.1096/fasebj.29.1_supplement.570.5" @default.
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