So long-chain fatty acids are dependent on the carnitine shuttle to enter the mitochondria but I read that short chain fatty acids do not require carnitines. I was wondering how and where short-chain carnitines are formed and what their roles are.
Malonyl-CoA is formed when acetyl-CoA is rich by acetyl-CoA carboxylase, meaning enough energy state. Malonyl-CoA potently inhibit CPT-1, resulting inhibition beta-oxidation. So, exceed acetyl-CoA is utilized for fat synthesis. Tiglyl-CoA is formed in the metabolism of isoleucine. These short-chain acyl-CoA inhibit mitochondrial function such as beta-oxidation. Accumulation of acyl-CoA inhibit mitochondrial function, it causes serious clinical problems, such as Reye's syndrome. If free carnitine is enough in mitochondria, carnitine takes these acyl group, such as malonyl, tiglyl, and palmytoyl, and form acylcarnitine, such as malonyl carnitine, tiglylcarnitine and palmytoylcarnitine, and these acylcarnitine is exported from inside of mitochondria, and finally are excreted in the urine. The mitochondrial function will be kept by carnitine. Carnitine is not needed to import short chain acyl group such as malonyl or tiglyl, but needs to export harmful acyl-group from mitochondria. Too high ratio of acyl-CoA/free CoA is resulting too high acylcarnitine/free carnitine, this is called as carnitine insufficiency.
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