Abstract
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.
Highlights
S-adenosylmethionine (SAMe) is a pleiotropic endogenous metabolite acting as a co-substrate in transmethylation, transsulfuration, and aminopropylation reactions [1]
We assessed the baseline effect of SAMe on lipid accumulation by exposing control FaO cells to SAMe and did not observe any significant effect (Figure S2 of Supplementary data)
The present in vitro study demonstrated a direct effect of SAMe in ameliorating fatty acid-induced steatosis and oxidative stress in hepatic and endothelial cells, and clarified some molecular mechanisms sustaining these effects
Summary
S-adenosylmethionine (SAMe) is a pleiotropic endogenous metabolite acting as a co-substrate in transmethylation, transsulfuration, and aminopropylation reactions [1]. SAMe is the most important methyl donor in mammalian cells, where it transfers a methyl group to acceptor molecules, such as DNA, proteins, and lipids, modifying their structure and function [5]. Many reports have shown that SAMe treatment causes the hypermethylation of DNA, which is typically associated with the silencing of gene expression [6]. For this reason, SAMe has been proposed for use in cancer therapy to reduce tumor development, Molecules 2020, 25, 4237; doi:10.3390/molecules25184237 www.mdpi.com/journal/molecules. Molecules 2020, 25, 4237 growth, and metastasis. SAMe protects against oxidative stress as it is a precursor for cysteine, which is one of the amino acids of glutathione (GSH), and the major physiological defense against reactive oxygen species (ROS) [7]
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