The acetyl-CoA enters the citric acid cycle, eventually forming several equivalents of ATP.
[1] The oxidative degradation of fatty acids is a two-step process, catalyzed by acyl-CoA synthetase.
Enoyl-CoA hydrase catalyzes the addition of water across the newly formed double bond to make an alcohol.
[6] This four step process repeats until acyl-CoA has removed all carbons from the chain, leaving only Acetyl-CoA.
Cellular acyl-CoA content correlates with insulin resistance, suggesting that it can mediate lipotoxicity in non-adipose tissues.
[11] Acyl-CoA: diacylglycerol acyltransferase (DGAT) plays an important role in energy metabolism on account of key enzyme in triglyceride biosynthesis.
The synthetic role of DGAT in adipose tissue such as the liver and the intestine, sites where endogenous levels of its activity and triglyceride synthesis are high and comparatively clear.
[12] A rare disease called multiple acyl-CoA dehydrogenase deficiency (MADD)[13] is a fatty acid metabolism disorder.
MADD is a genetic disorder, caused by a mutation in the ETFA, ETFB, and ETFDH genes.