Acyl-CoA dehydrogenase (VLCAD/LCAD/MCAD/SCAD)
Cofactors used
Clinical / pharmacological. MCAD deficiency: hypoketotic hypoglycaemia, dicarboxylic aciduria, SIDS-like presentation
What it does, reaction by reaction
Beta-Oxidation of Fatty Acids Lipid Metabolism · Mitochondrial matrix (peroxisome for VLCFA)
Fatty acyl-CoA + FAD → trans-Δ2-enoyl-CoA + FADH2
Converts Fatty acyl-CoA FAD into trans-Delta-2-Enoyl-CoA FADH2
› Notes
An acyl-CoA dehydrogenase catalyzes the first recurring oxidation. Very-long-, long-, medium-, or short-chain acyl-CoA dehydrogenase is selected by chain length; electrons pass from FADH2 through electron-transfer flavoprotein (ETF) and ETF:ubiquinone oxidoreductase to the ubiquinone pool. This is not directly ATP-producing but yields respiratory-chain reducing equivalents.
Showing all 1 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Beta-Oxidation of Fatty Acids
Listed there as: Acyl-CoA dehydrogenases (including MCAD)
ADP demand, NAD+/FAD regeneration, substrate supply
High NADH/NAD+ ratio; respiratory-chain impairment
Fasting hormones increase fatty-acid delivery; transcriptional control is mediated partly by PPARα in liver
Recent literature
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