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- Fatty acid oxidation pathway control state + ([[File:SUIT-catg F.jpg|right|300px|F-junct … [[File:SUIT-catg F.jpg|right|300px|F-junction]]</br>In the '''fatty acid oxidation pathway control state''' (F- or FAO-pathway), one or several fatty acids are supplied to feed electrons into the [[F-junction]] through fatty acyl CoA dehydrogenase (reduced form [[FADH2]]), to [[electron transferring flavoprotein]] (CETF), and further through the [[Q-junction]] to [[Complex III]] (CIII). FAO not only depends on electron transfer through the F-junction (which is typically rate-limiting relative to the N-pathway branch), but simultaneously generates FADH<sub>2</sub> and NADH and thus depends on [[N-junction]] throughput. Hence FAO can be inhibited completely by inhibition of [[Complex I]] (CI). In addition and independent of this source of NADH, the type N substrate malate is required at low concentration (0.1 mM) as a co-substrate for FAO in mt-preparations, since accumulation of Acetyl-CoA inhibits FAO in the absence of malate. Malate is oxidized in a reaction catalyzed by malate dehydrogenase to oxaloacetate (yielding NADH), which then stimulates the entry of Acetyl-CoA into the TCA cycle catalyzed by citrate synthase. Peroxysomal ''β''-oxidation carries out few ''β''-oxidation cycles, thus shortening very-long-chain fatty acids (>C<sub>20</sub>) for entry into mitochondrial ''β''-oxidation. Oxygen consumption by peroxisomal [[acyl-CoA oxidase]] is considered as [[residual oxygen consumption]] rather than cell respiration.esidual oxygen consumption]] rather than cell respiration.)
