Fatty acids are essential components of the human body, serving as a major source of energy, components of cell membranes, and precursors for various bioactive molecules. Understanding fatty acid metabolism is therefore crucial for maintaining overall health and preventing metabolic disorders. Fatty acids are long-chain hydrocarbons with a carboxylic acid group at one end. They can be classified based on their saturation status into three main types: saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs). SFAs have no double bonds between carbon atoms, MUFAs have one double bond, and PUFAs have multiple double bonds. Endogenous fatty acid synthesis primarily occurs in the liver, where excess carbohydrates and proteins are converted into fatty acids through de novo lipogenesis. Before entering metabolic pathways, fatty acids need to be activated to form acyl-CoA derivatives by attachment of a coenzyme A (CoA) molecule to the fatty acid, forming acyl-CoA. The activation step occurs in the cytoplasm for short- and medium-chain fatty acids, whilst long-chain fatty acids are transported to mitochondria for activation. β-oxidation is the primary pathway for fatty acid catabolism in humans. It takes place in the mitochondria and involves the sequential removal of two-carbon units from the acyl-CoA chain. Mitochondrial transport is facilitated by the carnitine shuttle system. The fatty acyl-CoA molecule is transferred from CoA to carnitine on the outer mitochondrial membrane, forming acyl-carnitine. The acyl-carnitine is then transported across the inner mitochondrial membrane into the mitochondrial matrix. Once inside the mitochondrial matrix, the beta-oxidation cycle begins, involving four main steps, which are repeated until the fatty acid is fully broken down into acetyl-CoA molecules. The first step of the beta-oxidation cycle involves the oxidation of the fatty acyl-CoA molecule. Here, acyl-CoA dehydrogenase catalyses the removal of two hydrogen atoms from the beta-carbon of the fatty acid, resulting in the formation of a trans double bond between the alpha and beta carbons, creating a trans-Δ2-enoyl-CoA molecule. The trans-Δ2-enoyl-CoA molecule then undergoes hydration with enoyl-CoA hydratase, resulting in the formation of a β-hydroxyacyl-CoA molecule. The β-hydroxyacyl-CoA is further oxidized in the third step by β-hydroxyacyl-CoA dehydrogenase, removing two hydrogen atoms from the β-hydroxyacyl-CoA molecule, regenerating the trans double bond, and forming a ketoacyl-CoA molecule. Finally, thiolase breaks the ketoacyl-CoA molecule into two parts: a two-carbon acetyl-CoA molecule and a shorter acyl-CoA molecule with two fewer carbons. The shorter acyl-CoA molecule is now ready to enter the beta-oxidation cycle again, starting with the oxidation step and the cycle repeated until the entire fatty acid is broken down into multiple acetyl-CoA molecules which then enter the citric acid cycle to further generate ATP through oxidative phosphorylation. Conversely, fatty acid synthesis (lipogenesis) occurs in the cytoplasm and involves the addition of two-carbon units to the growing fatty acid chain by fatty acid synthase (FAS). Acetyl-CoA carboxylase (ACC) is another key lipogenic enzyme that converts acetyl-CoA to malonyl-CoA, which serves as a building block for fatty acid synthesis. We offer a comprehensive product range of research reagents for investigating fatty acid metabolism, including Adiponectin antibodies, FABP4 antibodies, MC3 Receptor antibodies, Adiponectin ELISA Kits, and Leptin Receptor ELISA Kits. Explore our full fatty acid metabolism product range below and discover more, for less.