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| Section2 = }} Triacsin C is a potent inhibitor of long fatty acyl CoA synthetase. It blocks β-cell apoptosis, induced by fatty acids (lipoapoptosis) in a rat model of obesity. In addition, it blocks the de novo synthesis of triglycerides, diglycerides, and cholesterol esters, thus interfering with lipid metabolism. In addition, triacsin C is a potent vasodilator. Inhibition of lipid metabolism reduces/removes lipid droplets from HuH7 cells. In hepatitis C infected HuH7 cells, this reduction/removal of lipid droplets significantly reduces virion formation and release. ==General chemical description== Triacsin C belongs to a family of fungal metabolites all having an 11-carbon alkenyl chain with a common ''N''-hydroxytriazene moiety at the terminus. Due to the ''N''-hydroxytriazene group, triacsin C has acidic properties and may be considered a polyunsaturated fatty acid analog. Triacsin C was discovered by Yoshida K, and other Japanese scientists, in 1982, in a culture of the microbe ''Streptomyces aureofaciens''. They identified it as a vasodilator. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Triacsin C」の詳細全文を読む スポンサード リンク
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