Fatty-acyl-CoA synthase
Fatty acids are key components of a cell, therefore, the regulation or inhibition of fatty acid synthesis hold severe consequences for cellular function. The malfunction of the fatty acid synthesis pathway can result in cancer and obesity. However, the significance of fatty acid synthesis also make the fatty acid synthesis pathway a potential target for the search and study of anticancer and antibiotic drugs. It has been found that in humans, fatty acid synthase, is overly expressed in cancer cells. Therefore, FAS, which has been associated only with energy production prior, is now associated with aggressive tumor growth and survival. Studies have also found that human fatty acid synthase is overly expressed in prostate cancer cells.
Lipid
Beta oxidation is the metabolic process by which fatty acids are broken down in the mitochondria or in peroxisomes to generate acetyl-CoA. For the most part, fatty acids are oxidized by a mechanism that is similar to, but not identical with, a reversal of the process of fatty acid synthesis. That is, two-carbon fragments are removed sequentially from the carboxyl end of the acid after steps of dehydrogenation, hydration, and oxidation to form a beta-keto acid, which is split by thiolysis. The acetyl-CoA is then ultimately converted into ATP, CO, and HO using the citric acid cycle and the electron transport chain. Hence the citric acid cycle can start at acetyl-CoA when fat is being broken down for energy if there is little or no glucose available. The energy yield of the complete oxidation of the fatty acid palmitate is 106 ATP. Unsaturated and odd-chain fatty acids require additional enzymatic steps for degradation.