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The fatty acid metabolism pathway, also known as lipid catabolism/anabolism, refers to a network of biochemical reactions responsible for the breakdown (beta‑oxidation) and synthesis (lipogenesis) of fatty acids. This process involves numerous enzymes—such as acyl-CoA dehydrogenases, carnitine palmitoyltransferases, acetyl-CoA carboxylases, and fatty acid synthases—that collectively regulate cellular energy supply by converting fats into ATP or storing excess energy in lipid form. The regulation occurs at multiple points via hormones like insulin/glucagon and through substrate availability. Disruption in this network contributes to diseases including obesity, diabetes mellitus, cardiovascular disease, cancer progression/metastasis, among others[1][2][3][4]. Because it describes an entire *pathway* rather than a single molecule/protein/receptor/enzyme/transporter/etc., it is not considered an individual therapeutic target; instead drug development focuses on specific nodes within this system.
Mechanisms depend on the enzyme targeted: Inhibition of fatty acid oxidation by blocking CPT1 reduces energy production from fats. Inhibition of fatty acid synthase blocks de novo lipogenesis. Modulation of acetyl-CoA carboxylase affects malonyl-CoA levels and thus both synthesis and oxidation rates.
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