肠道菌群的代谢产物三甲胺-N-氧化物(trimethylamine-N-oxide,TMAO)是一种新发现的心血管疾病的危险因子.肠道菌群利用食物中的胆碱和左旋肉碱转化为三甲胺(trimethylamine,TMA),三甲胺在肝酶中氧化为TMAO,降低TMA可以刺激巨噬细胞逆向转运胆固醇和抑制动脉粥样硬化形成.TMAO生成素单加氧酶3(flavin-containing monooxygenase 3,FMO3)是胆固醇代谢和胆固醇逆向转运的工具,降低FMO3可以减缓胆囊分泌胆汁,延缓肠道对胆固醇的吸收,并限制合成氧化型胆固醇和胆固醇酯.血液中TMAO可上调巨噬细胞内的清道夫受体,促使巨噬细胞内胆固醇累积和泡沫细胞的形成,进而促进血管斑块的形成并通过MAPK和细胞核因子κB通路促进血管炎性反应.TMAO集中作用于影响胆固醇代谢、胰岛素抵抗、促进血小板高聚集、增加血栓形成、促进血管炎症反应及直接导致动脉斑块形成等方面.降低TMAO水平可以潜在的预防或治疗动脉粥样硬化相关疾病,降低心脑血管疾病发病率.TMA/FMO3/TMAO通路是调节脂质代谢和炎症的主要通路.%Trimethylamine-N-oxide (TMAO),metabolites of the intestinal microflora,is a newly discovered risk factor for cardiovascular disease.The intestinal flora converted choline and L-carnitine into trimethylamine in the food.Trimethylamine is oxidized to TMAO in liver enzymes.Lowering TMA can stimulate macrophages to reverse cholesterol transport and inhibit atherogenesis.TMAO poietin-monooxygenase 3 (FMO3) is a tool for cholesterol metabolism and reverse cholesterol transpor,lowering FMO3 can slow the gallbladder's secretion of bile,delay intestinal absorption of cholesterol,and limit the synthesis of oxidized cholesterol and cholesterol esters.TMAO in the blood can up regulate scavenger receptors in macrophages,and promote accumulation of cholesterol and formation of foam cells in macrophages,thereby promoting vascular plaque formation and promote the inflammatory response by MAPK and nuclear factor kappa B pathway.TMAO concentrates on affecting cholesterol metabolism,increasing insulin resistance,promoting platelet aggregation,increasing thrombosis,promoting vascular inflammatory response and directly leading to the formation of atherosclerotic plaques.Lowering TMAO levels can potentially prevent or treat atherosclerotic related diseases and reduce the incidence of cardiovascular and cerebrovascular diseases.The intestinal flora of the TMA/FMO3/TMAO pathway is the major pathway regulating lipid metabolism and inflammation.
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