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 metabolism
In the cytosol of the cell (for example a muscle cell), the glycerol will be converted to glyceraldehyde 3-phosphate, which is an intermediate in the glycolysis, to get further oxidized and produce energy. However, the main steps of fatty acids catabolism occur in the mitochondria. Long chain fatty acids (more than 14 carbon) need to be converted to Fatty acyl-CoA in order to pass across the mitochondria membrane. Fatty acid catabolism begins in the cytoplasm of cells as Acyl-CoA synthetase uses the energy from cleavage of an ATP to catalyze the addition of Coenzyme A to the fatty acid. The resulting Acyl-CoA cross the mitochondria membrane and enter the process of beta oxidation. The main products of the beta oxidation pathway are Acetyl-CoA (which is used in the Citric acid cycle to produce energy), NADH and FADH. The process of beta oxidation requires the following enzymes: Acyl CoA dehydrogenase, Enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase. The diagram to the left shows how fatty acids are converted into Acetyl-coA. The overall net reaction, using palmitoyl CoA (16:0) as a model substrate is: