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The **liver peroxisomal beta-oxidation pathway** is a series of enzymatic reactions occurring within hepatic peroxisomes, primarily responsible for shortening very long-chain, branched fatty acids, and some prostaglandins/leukotrienes. These fatty acids cannot be metabolized by mitochondria due to their length, so peroxisomes initiate their breakdown, ultimately producing acetyl-CoA and hydrogen peroxide (H2O2)[2][1]. Key enzymes include **acyl-CoA oxidase (Acox1)**, which performs the initial oxidation, and **PPARα** regulates the expression of these enzymes[1][2][4]. The pathway is distinct from mitochondrial beta-oxidation, as it is not directly coupled to ATP synthesis and contributes to the production of reactive oxygen species. Dysfunction or genetic deficiency of pathway enzymes can drive fatty liver pathology, steatohepatitis, and overall dysregulation of metabolism and immune responses[3][1].
Induction of pathway enzymes (by activating PPARα, increasing fatty acid oxidation and decreasing lipid accumulation)
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