Mutations in the ACADVL gene lead to inadequate levels of an enzyme called very<unk> -chain acyl-coenzyme A (CoA) dehydrogenase. Without this enzyme,<unk> -chain fatty acids from food and fats stored in the body cannot be degraded and processed. As a result, these fatty acids are not converted into energy, which can lead to characteristic signs and symptoms of this disorder, such as lethargy and hypoglycemia. Levels of very<unk> -chain fatty acids or partially degraded fatty acids may build up in tissues and can damage the heart, liver, and muscles, causing more serious complications. VLCAD<unk>  is characterized as an inherited genetic disorder. The mutations that occur within the gene itself are recessive, meaning that an individual has to acquire both recessive mutated genes in order for the disease to manifest. There are various forms of the disease that can be manifested in infancy, adolescence, and adulthood. However, it is still unknown at to what causes the disease to manifest itself in the different life stages.
Very long-chain acyl-coenzyme A dehydrogenase deficiency
Short-chain acyl-coenzyme A dehydrogenase deficiency
2-Methylbutyryl-CoA dehydrogenase deficiency
3-hydroxyacyl-coenzyme A dehydrogenase deficiency
3-Methylcrotonyl-CoA carboxylase deficiency
Succinyl-CoA:3-oxoacid CoA transferase deficiency
Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency
Medium-chain acyl-coenzyme A dehydrogenase deficiency