TY - JOUR TI - New Perspectives of S-Adenosylmethionine (SAMe) Applications to Attenuate Fatty Acid-Induced Steatosis and Oxidative Stress in Hepatic and Endothelial Cells AU - Vergani, Laura AU - Baldini, Francesca AU - Khalil, Mohamad AU - Voci, Adriana AU - Putignano, Pietro AU - Miraglia, Niccolò T2 - Molecules AB - S-adenosylmethionine (SAMe) is an endogenous methyl donor derived from ATP and methionine that has pleiotropic functions. Most SAMe is synthetized and consumed in the liver, where it acts as the main methylating agent and in protection against the free radical toxicity. Previous studies have shown that the administration of SAMe as a supernutrient exerted many beneficial effects in various tissues, mainly in the liver. In the present study, we aimed to clarify the direct effects of SAMe on fatty acid-induced steatosis and oxidative stress in hepatic and endothelial cells. Hepatoma FaO cells and endothelial HECV cells exposed to a mixture of oleate/palmitate are reliable models for hepatic steatosis and endothelium dysfunction, respectively. Our findings indicate that SAMe was able to significantly ameliorate lipid accumulation and oxidative stress in hepatic cells, mainly through promoting mitochondrial fatty acid entry for β-oxidation and external triglyceride release. SAMe also reverted both lipid accumulation and oxidant production (i.e., ROS and NO) in endothelial cells. In conclusion, these outcomes suggest promising beneficial applications of SAMe as a nutraceutical for metabolic disorders occurring in fatty liver and endothelium dysfunction. DA - 2020/01// PY - 2020 DO - 10.3390/molecules25184237 DP - www.mdpi.com VL - 25 IS - 18 SP - 4237 LA - en UR - https://www.mdpi.com/1420-3049/25/18/4237 Y2 - 2020/09/18/18:28:29 KW - S-adenosylmethionine (SAMe) KW - atherosclerosis KW - endothelium dysfunction KW - non-alcoholic fatty liver disease KW - oxidative stress KW - steatosis ER -