PTEN down-regulation by unsaturated fatty acids triggers hepatic steatosis via an NF-κBp65/mTOR-dependent mechanism

摘要: Background & Aims: Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor regulator of insulin sensitivity in peripheral tissues. In the liver, PTEN deletion increases sensitivity, but induces steatosis, steatohepatitis, hepatocellular carcinoma. Here, we investigated pathophysiologic mechanisms regulating expression liver development steatosis. Methods: was evaluated rats human beings having metabolic syndrome. Signaling pathways lipid accumulation hepatocytes were examined vitro. Results: down-regulated steatosis high plasma levels fatty acids, as well steatotic livers. Unsaturated acids inhibited HepG2 cells via activation signaling complex formed by mammalian target rapamycin (mTOR) nuclear factor-κB (NF-κB). Down-regulation induced affecting import, esterification, extracellular release acids. Conclusions: Hepatic can be mediated alterations exposed to unsaturated Furthermore, our data revealed interaction between mTOR NF-κB, suggesting cross-talk these 2 pathways.