4.5 Article

Taurine alleviated hepatic steatosis in oleic acid-treated-HepG2 cells and rats fed a high-fat diet

Journal

HELIYON
Volume 9, Issue 6, Pages -

Publisher

CELL PRESS
DOI: 10.1016/j.heliyon.2023.e16401

Keywords

Taurine; AMP -activated protein kinase (AMPK); Triacylglycerol; Hepatic steatosis

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Taurine has been shown to alleviate symptoms of metabolic associated fatty liver disease. This study investigated its protective effect for hepatic steatosis and its modulation of the AMP-activated protein kinase and insulin signaling pathway.
Taurine has been proven in many trials to alleviate the symptoms of metabolic associated fatty liver disease. Here its protective effect for hepatic steatosis and modulation of AMP-activated protein kinase and insulin signaling pathway were investigated. Steatotic HepG2 cell estab-lished with oleic acid (0.05 mmol/L), treated with taurine (5 mmol/L), dorsomorphin (10 & mu;mol/ L) for 24 h. Sprague Dawley rats were divided into regular and high-fat diet (HFD) groups, and their corresponding taurine (70 or 350 mg/kg BW/d) groups, fed for 8 weeks. In steatotic cell, taurine reduced the TG concentration and SREBP-1c, PPAR & gamma;, FAS, ACC, SCD1 protein levels, decreased phosphorylation of mTOR, IRS1 (Ser302), increased phosphorylation of AMPK & alpha;, LKB1, PI3K, Akt, ACC. While dorsomorphin eliminated taurine's TG-lowering effect. In HFD-fed rats, taurine reduced liver TG, serum TG, ALT, AST, IL-1 & beta;, IL-4, TNF-& alpha;. The effects of taurine on the main factors of fatty acid synthesis were mostly consistent with cell experiments, and the reduction of microRNAs (451, 33, 291b) was aligned with the improvement in LKB1 and AMPK expression in HFD rats. Taurine alleviated steatosis-induced inhibition of IRS1-PI3K-Akt pathway, but suppressed its positively regulated downstream factor mTOR. In parallel, taurine reduced steatosis by activating LKB1-AMPK & alpha; pathway via phosphorylation and no-phosphorylation manner, then inhibiting SREBP-1c directly or by suppressing mTOR phosphorylation.

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