Hepatic fatty acid oxidation pathway

The **hepatic fatty acid oxidation pathway** refers collectively to a series of enzymatic reactions in the liver that break down long-chain fatty acids for energy production. This process is essential for maintaining energy balance during fasting and involves several steps and key proteins. Fatty acids enter hepatocytes via transporters such as CD36/FAT and FATP. Once inside, they are activated by acyl-CoA synthase and transported into mitochondria through the carnitine shuttle system involving carnitine palmitoyltransferase 1 (CPT1), carnitine-acylcarnitine translocase, and CPT2[1][3]. Within mitochondria, **β‑oxidation** sequentially removes two-carbon units from acyl-CoA molecules as acetyl-CoA using a cycle catalyzed by dehydrogenases, hydratases, and thiolases[2][3]. Acetyl-CoA then enters the tricarboxylic acid cycle or is used for ketone body synthesis during prolonged fasting[4]. Defects in this multi-enzyme process can lead to severe metabolic diseases including hypoglycemia and hepatic steatosis. Note: "Hepatic fatty acid oxidation pathways" is not a single molecular target but rather describes an entire class of biochemical processes involving many different proteins/enzymes. It does not fit standard definitions for therapeutic targets like receptors or enzymes; thus it should be flagged as *not* a canonical target entity suitable for structured drug-target databases[1][2][3].

Other names

Liver fatty acid oxidationFatty acid β-oxidation in liverHepatic β-oxidation

Mechanisms would depend on specific enzyme targets within the pathway, e.g., inhibition of CPT1 to reduce hepatic ketogenesis