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Fatty Acid Oxidation Assay Kit



(FAO Assay Kit)



Product Description:

Fatty acids provide more ATP per carbon than carbohydrates such as glucose. In tissues with high energy requirement, such as heart, up to 50 – 70% of energy comes from fatty acid beta-oxidation, which converts fatty acids to acetyl-CoA with concomitant production of FADH2 and NADH in the mitochondria. This strictly aerobic oxidative pathway consists of four distinct steps: acyl-CoA dehydrogenation by acyl- CoA dehydrogenase, hydration by enoyl-CoA hydratase, dehydrogenation by 3-hydroxyacyl-CoA dehydrogenase, and thiolytic cleavage by beta- ketothiolase. The importance of the beta-oxidation system in humans is exemplified by the existence of a group of genetic diseases categorized as fatty acid oxidation disorders (FAODs), which are a heterogeneous group of defects in fatty acid transport and oxidation, and are inherited as autosomal recessive disorders, having a wide range of clinical presentations. In addition, evidence indicates that regulation of activity of FAO during fetal development is not only important for fetal life but also has implications for health and disease in adulthood. The measurement of FAO activity thus provides valuable insights into the pathophysiologic and metabolic basis of many diseases. The non-radioactive FAO assay is based on oxidation of the substrate octanoyl-CoA. Generation of NADH is coupled to the reduction of the tetrazolium salt INT to formazan. The intensity of the red-colored formazan is proportional to increased FAO activity. The assay solution and substrate should be stored in aliquots at -80ºC.

#Fatty Acid Oxidation​


Kit Components:

FAO Assay Solution: 5 ml, store at -70°C (for 100 wells)

20x Octanoyl-CoA: 0.25 ml, store at -70ºC

10x Cell Lysis Solution: 25 ml, store at 4ºC


SDS:

DMSO, INT, Tris


Related Kits:

HK Enzyme Assay, G6PD Enzyme Assay, Adenylate Kinase Assay


Citation:

Kwong et al

Metabolic role of fatty acid binding protein 7 in mediating triple-negative breast cancer cell death via PPAR-alpha signaling

J. Lipid Res. 60:1807, 2019


Cheng et al

Targeting DGAT1 ameliorates glioblastoma by increasing fat catabolism and oxidative stress

Cell Metabolism 32, 229-242, 2020


Chen et al

HNF4 regulates fatty acid oxidation and is required for renewal of intestinal stem cells in mice

Gastroenterology 158(4):985-999, 2020


Veeriah et al

Long-term oral administration of an HNF4α agonist prevents weight gain and hepatic steatosis by promoting increased mitochondrial mass and function

Cell Death & Disease 13(1):89, 2022


Xu et al

Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α

Theranostics 12(6):2502-2518, 2022


Huang et al

PERM1 regulates genes involved in fatty acid metabolism in the heart by interacting with PPARα and PGC‑1α

Scientific Reports 12:14576, 2022