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The peroxisomal and mitochondrial β-oxidation pathway is a fundamental metabolic route in eukaryotic cells responsible for degrading fatty acids via successive removal of two-carbon acetyl-CoA units. In mitochondria, medium- and long-chain fatty acids undergo β-oxidation coupled with ATP synthesis, while peroxisomes preferentially oxidize very long-chain and branched fatty acids, generating hydrogen peroxide instead of ATP. The pathway involves a series of distinct but parallel enzymatic steps in each organelle, including activation of fatty acids, transport into the organelle, and sequential oxidation via dehydrogenases, oxidases, and thiolases. Disorders of these processes lead to energy deficiency, lipid accumulation, and toxic metabolite buildup, underlying many inherited and acquired metabolic diseases. Pharmacological manipulation of these pathways is used to treat certain lipid disorders and to probe metabolic flux in research settings[1][2][3][4].
Induction of fatty acid oxidation enzymes via receptor activation (e.g., clofibrate acting via PPARα) Inhibition of fatty acid transport into mitochondria (etomoxir inhibits CPT1) Scavenging of reactive oxygen species (antioxidants like NACA restore redox balance) Modulation of peroxisomal ROS and downstream lipolysis
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