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There are a bunch of other inborn errors of metabolism, including short-chain acyl-CoA dehydrogenase deficiency and medium-chain acyl-CoA dehydrogenase deficiency.[ref] Lets look at the inborn errors of metabolism involving carnitine: CPT2 gene: The CPT2 gene encodes the enzyme that moves fatty acids attached to carnitine into the inner membrane of the mitochondria

However, isotope tracer studies confirm that TMA and TMAO are sequentially made from orally ingested l-carnitine in both mice and humans, and l-carnitine supplementation has been shown to accelerate atherosclerosis development in murine models of the disease (6, 26)

Binding and Degradation of Low Density Lipoproteins by Cultured Human Fibroblasts: comparison of cells from a normal subject and from a patient with homozygous familial hypercholesterolemia

The success of carnitine therapy in ischemic heart disease was first attributed to the higher in fat oxidation in cardiac myocytes, which resulted in an increased energy supply

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