Triacsin C is an inhibitor of long fatty acyl CoA synthetase that has been isolated from Streptomyces aureofaciens. 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 vasodilator. Inhibition of lipid metabolism reduces/removes lipid droplets from HuH7 cells. In hepatitis C–infected HuH7 cells, this reduction/removal of lipid droplets by triacsin C correlates with a reduction in virion assembly and infectivity.
General chemical description Triacsin C belongs to a family of bacterial secondary metabolites all having an 11-carbon 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 a group led by Keizo Yoshida in 1982 from a culture of the actinobacteria now known as Kitasatospora aureofaciens.
See also Fatty acid degradation#Activation_and_transport_into_mitochondria Fatty acyl CoA synthetase
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