dehydrogenaseacetylCoA

DehydrogenaseacetylCoA is not a standard enzyme name in biochemical databases. The phrase most often points to enzymes in the acyl-CoA dehydrogenase (ACAD) family, which catalyze the first oxidation step of fatty acid beta-oxidation. In this context, substrates are fatty acyl-CoAs of varying chain lengths, and the reaction converts an acyl-CoA to a trans-2-enoyl-CoA with the concomitant reduction of FAD to FADH2. The electrons are subsequently transferred to the electron-transferring flavoprotein (ETF) and then to the respiratory chain. Acetyl-CoA itself is typically a product of beta-oxidation, not a substrate for the acyl-CoA dehydrogenases, although the overall pathway produces acetyl-CoA from longer-chain fatty acids.

Acyl-CoA dehydrogenases are located mainly in the mitochondrial matrix in eukaryotes; peroxisomal variants handle specific substrates, notably very long-chain acyl-CoAs. They share a flavin adenine dinucleotide (FAD) binding domain and commonly form homodimers or higher-order oligomers. The ACAD enzyme family is diverse, with different members displaying chain-length preferences (short-, medium-, long-, and very-long-chain acyl-CoA dehydrogenases).

Genetic defects in ACAD family members cause fatty acid oxidation disorders (FAODs), such as medium-chain acyl-CoA dehydrogenase deficiency (MCAD) and very long-chain acyl-CoA dehydrogenase deficiency (VLCAD). These conditions affect energy metabolism, particularly during fasting or illness, and are detected by newborn screening and biochemical tests.

In summary, while the exact term dehydrogenaseacetylCoA is not a widely used enzyme name, it commonly refers to the acyl-CoA dehydrogenase family that initiates fatty acid beta-oxidation. See also beta-oxidation, acyl-CoA dehydrogenase, ETF, MCAD deficiency, and VLCAD deficiency.