Acyl-CoAs Profile Service

Acyl-CoAs Profile Service

Acyl-coenzyme A (Acyl-CoA) is a family of coenzymes involved in the metabolism of fatty acids. It is a  temporary compound formed when CoA attaches to the end of a long-chain fatty  acid in living cells. This compound undergoes beta oxidation, forming at least one  molecules of acetyl-CoA. This, in turn, enters the citric acid cycle, finally forming  several molecules of ATP.

The oxidation of fatty  acids in the mitochondria gives rise to the generation of energy to be utilized when  there is an increased requirement for energy such as illness, fasting, and  muscular exertion. The biological process of fatty acid oxidation (FAO)  includes the carnitine cycle, the betaoxidation cycle, the electron-transport  chain, and, in liver, ketone synthesis. Free fatty acids are activated to their  CoA esters in the cytosol at the outer mitochondrial membrane. Long-chain (C16  and C18) fatty acyl-CoAs enter the mitochondria as acylcarnitines and are  reconverted back to their respective acyl-CoA's at the mitochondrial membrane.

With each step of FAO,  fatty acyl-CoAs are chain-shortened by two carbons until fully converted to  acetyl-CoA. Transfer of energy released during beta-oxidation to the electron  transport chain results in the generation of adenosine triphosphate (ATP). In  the liver, most of the acetyl-CoA is applied to synthesize ketone bodies  (3-hydroxybutyrate and acetoacetate), which can be utilized as fuel by tissues  that are unable to oxidize fatty acids, most remarkably, the brain. Fatty acids  can be directly used by tissues such as cardiac and skeletal muscle as a source  of energy. Disorders in FAO can result in various phenotypes including brain  damage, hypoglycemia, kidney dysfunction, liver disease, and damage to cardiac  and skeletal muscle.

Early detection of FAO  disorders is important to ensure that the proper evaluation and management are carried  out in a timely fashion. The major accumulating metabolites in fatty acid  oxidation defects are intramitochondrial acyl-CoAs. Usually, secondary  metabolites such as acylcarnitines, acylglycines and dicarboxylic acids are  measured to study these defects. Most published approaches involve HPLC  separations and all previously published approaches do not detect a complete range  of acyl-CoA species, primarily due to hydrophobicity differences between long-,  medium- and short-chain acyl-CoA species. An analytical approach has been  developed by Andrew A. Palladino to directly measure diverse fatty acyl-CoA  species of all chain lengths using flow-injection tandem MS. This method was evaluated  using liver from the short-chain-acyl-CoA dehydrogenase deficient mouse and  tested with the medium- and short-chain-3-hydroxyacyl-CoA dehydrogenase knock  out mouse.

Currently, a reliable and  reproducible method using highly  sensitive LC-MS/MS platform for the  identification and quantification of diverse  acyl-CoA species in different sample types has been established by the  scientists at Creative Proteomics, which can satisfy the needs of academic and industrial  study in your lab.


 Identification and  quantification of diverse acyl-CoA species by mixed organic solvent extraction. Then,  extracts are dried, re-suspended for LC/MS separation and measured on a LC-MS  mass spectrometer using MRM methods.

Sample  Requirement


Representative acyl-CoA species that can be measured by targeted LC-MS/MS

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Acyl-CoAs Profile Service

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Staffed by experienced biological  scientists, Creative Proteomics can provide a wide range of services ranging from the  sample preparation to the lipid extraction, characterization, identification and quantification. We promise  accurate and reliable analysis, in  shorter duration of time! You are welcome to discuss your  project with us.

* For Research Use Only. Not for use in diagnostic procedures.
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