ACADL is a gene that encodes LCAD - acyl-CoA dehydrogenase, long chain - which is a member of the acyl-CoA dehydrogenase family. The acyl-CoA dehydrogenase family is primarily responsible for beta-oxidation of fatty acids within the mitochondria. LCAD dysfunction is associated with lowered fatty acid oxidation capacity and decreased heat generation. As a result, LCAD deficiency has been correlated with increased cardiac hypertrophy, pulmonary disease, and overall insulin resistance. The LCAD enzyme catalyzes most of fatty acid beta-oxidation by forming a C2-C3 trans-double bond in the fatty acid. LCAD works on long-chain fatty acids, typically between C12 and C16-acylCoA. LCAD is essential for oxidizing unsaturated fatty acids such as oleic acid, but seems redundant in the oxidation of saturated fatty acids. Fatty acid oxidation has proven to spare glucose in fasting conditions, and is also required for amino acid metabolism, which is essential for the maintenance of adequate glucose production. LCAD is regulated by a reversible acetylation mechanism by SIRT3, in which the active form of the enzyme is deacetylated, and hyperacetylation reduces the enzymatic activity.