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Overview of the synthase cycle: (1) Activation (apo→holo) of the FAS by ACPS, (2) priming with Acetyl-CoA by AT, (3) transfer of the acetyl group from the ACP to the active site of the KS, (4) transacylation of the ACP with Maloyl-CoA by MPT, Claisen condensation at the KS by (5) decarboxylation and (6) nucleophilic attack of the enolate at ...
Lipogenesis inhibitor is a class of drug that works by inhibiting de novo lipogenesis—the generation of fatty acids in the body. These drugs target enzymes involved in lipogenesis, such as citrate/isocitrate carrier (CIC), ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS).
CPT-I inhibitors: etomoxir, oxfenicine, perhexiline CPT-I (carnitine palmitoyl transferase) converts fatty acyl-CoA to fatty acyl-carnitine. Carnitine biosynthesis inhibitor: mildronate [1] 3-KAT inhibitors: trimetazidine 3-KAT (3-ketoacyl-coenzyme A thiolase) inhibitors directly inhibits fatty acid beta-oxidation.
Cerulenin is an antifungal antibiotic that inhibits fatty acid and steroid biosynthesis.It was the first natural product antibiotic known to inhibit lipid synthesis. [1] In fatty acid synthesis, it has been reported to bind in equimolar ratio to b-keto-acyl-ACP synthase, one of the seven moieties of fatty acid synthase, blocking the interaction of malonyl-CoA.
New effective drugs are needed to combat this disease. Inhibitors against mtFabH, or against other enzymes of the FAS-II pathway, may have broader utility, such as the treatment of multidrug-resistant Staphylococcus aureus, and Plasmodium falciparum, the causative agent of another serious refractory problem, malaria.
Triacsin C is an inhibitor of long fatty acyl CoA synthetase that has been isolated from Streptomyces aureofaciens. [1] [2] [3] It blocks β-cell apoptosis, induced by fatty acids (lipoapoptosis) in a rat model of obesity.
This inhibition is a good target for future attempts to regulate CPT1 for the treatment of metabolic disorders. [20] Acetyl-CoA carboxylase (ACC), the enzyme that catalyzes the formation of malonyl-CoA from acetyl-CoA, is important in the regulation of fatty acid metabolism.
ACC is a biotin-containing enzyme which catalyzes the carboxylation of acetyl-CoA to malonyl-CoA, the rate-limiting step in fatty acid synthesis. ACC-beta is thought to control fatty acid oxidation by means of the ability of malonyl-CoA to inhibit carnitine palmitoyltransferase I , the rate-limiting step in fatty acid uptake and oxidation by ...