Acylcarnitines: Role in brain - ScienceDirect.
Acylcarnitine translocase deficiency is an exceedingly rare defect. It was initially reported in a male infant who suffered a cardiac arrest at 36 hours of age in association with fasting stress and ventricular dysrhythmias (Roe and Ding, 2001; Stanley et al, 2006).
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Many eukaryotes have the ability to synthesize carnitine, including humans. Humans synthesize carnitine from the substrate TML (6- N -trimethyllysine), which is in turn derived from the methylation of the amino acid lysine.
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The synthesis of succinylcarnitine (C4DC, conventional nomenclature for an acyl carnitine of a four carbon dicarboxylic acid) from succinyl chloride has previously been shown (Bohmer and Bremer, 1968) to afford a product with only 70% purity.
Carnitine-acylcarnitine translocase is responsible for passive transport of carnitine and carnitine-fatty acid complexes and across the inner mitochondrial membrane as part of the carnitine shuttle system.
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The liver is the most important organ for endogenous carnitine synthesis and metabolism. Hepatocellular carcinoma (HCC), a primary malignancy of the live with poor prognosis, may strongly influence the level of acylcarnitines. In this paper, the function, detection and alteration of acylcarnitine metabolism in HCC were briefly reviewed.
Fatty acid synthesis and oxidation are inversely regulated so that when fatty acid synthesis is activated, the catabolism of fatty acids is turned-off. Malonyl-CoA, produced by acetyl-coenzyme A carboxylase, a key enzyme of cytosolic fatty acid synthesis, represents a regulator of both metabolic pathways.
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The mitochondrial acylcarnitine synthesis pathway is exposed to multiple fatty acid substrates present simultaneously in the cell milieu, with each fatty acid present at varying pool sizes. The selectivity of this pathway for any particular fatty acid substrate under conditions of multisubstrate availability has not yet been tested experimentally.
