fatty acid oxidation occurs at the cell membrane.
fatty acid oxidation occurs at the cell membrane.
where does fatty acid oxidation occur in the cell?
cell membrane
the carnitine-mediated entry process is a rate-limiting factor for fatty acid oxidation and is an important point of regulation.









































section::::regulation of fatty acid β oxidation.:inhibition.









































the liver starts actively making triglycerides from excess glucose when it is supplied with glucose that cannot be oxidized or stored as glycogen. this increases the concentration of malonyl-coa, the first intermediate in fatty acid synthesis, leading to the inhibition of carnitine acyltransferase 1, thereby preventing fatty acid entry into the mitochondrial matrix for β oxidation. this inhibition prevents fatty acid breakdown while synthesis is happening.









































section::::regulation of fatty acid β oxidation.:activation.
carnitine
mitochondria-mediated oxidative stress plays a role in cardiomyopathy in type 2 diabetics. increased fatty acid delivery to the heart increases fatty acid uptake by cardiomyocytes, resulting in increased fatty acid oxidation in these cells. this process increases the reducing equivalents available to the electron transport chain of the mitochondria, ultimately increasing reactive oxygen species (ros) production. ros increases uncoupling proteins (ucps) and potentiate proton leakage through the adenine nucleotide translocator (ant), the combination of which uncouples the mitochondria. uncoupling then increases oxygen consumption by the mitochondria, compounding the increase in fatty acid oxidation. this creates a vicious cycle of uncoupling; furthermore, even though oxygen consumption increases, atp synthesis does not increase proportionally because the mitochondria is uncoupled. less atp availability ultimately results in an energy deficit presenting as reduced cardiac efficiency and contractile dysfunction. to compound the problem, impaired sarcoplasmic reticulum calcium release and reduced mitochondrial reuptake limits peak cytosolic levels of the important signaling ion during muscle contraction. the decreased intra-mitochondrial calcium concentration increases dehydrogenase activation and atp synthesis. so in addition to lower atp synthesis due to fatty acid oxidation, atp synthesis is impaired by poor calcium signaling as well, causing cardiac problems for diabetics.
mitochondrion