Mitochondrial Long Chain Fatty Acid Oxidation Related Enzyme Changes in Different Preeclampsia-Like Mouse Models

Most fatty acids in the human body are long-chain fatty acids. The β-oxidation of fatty acids occurs in the mitochondria. After activation of long-chain fatty acids, they need assistance from carnitine as a carrier and catalysis of carnitine palmitoyltransferase I (CPT I) in the outer mitochondrial membrane and carnitine palmitoyltransferase II (CPT II) in the inner mitochondrial membrane to enter into the mitochondria [1]. Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) is a component of the mitochondrial trifunctional protein and is capable of catalyzing the third step of β-oxidation [2]. So CPT I, CPT II and LCHAD are key enzymes in the long-chain FAO process, and defects or dysfunction of which can result in disorders in longchain fatty acid transport into the mitochondria or oxidation, further resulting in inefficient energy release from FAO and affecting cell function.