Triglyceride accumulation in skeletal muscles boosts in subjects with insulin resistance. The increase of triglyceride accumulation is a direct result reduced mitochondrial fatty acid FK228 cost oxidation in cells. Fenofibrate was demonstrated to prevent the development of diabetes in obese diabetes inclined subjects, however the process isn’t completely comprehended. The cellular gas measure, 50 AMP activated protein kinase, a power indicator protein, is considered as a target for treating type 2 diabetes. Fenofibrate was shown to activate AMPK in human umbilical vein endothelial cells and retinal endothelial cells, but whether fenofibrate regulates lipid metabolism via an AMPK pathway hasn’t been examined in C2C12 myotubes. Activation of AMPK is well known to phosphorylate and inactivate the downstream protein, acetyl CoA carboxylase. ACC phosphorylation results in decreased malonyl CoA production and increased carnitine palmitoyltransferase 1 activity, which increases the transport of fatty acid into mitochondria for fatty acid t oxidation. ATGL, a discovered lipase, is responsible for triglyceride hydrolase activity in cells and is considered as a therapeutic target for dyslipidemia and fatty liver. Notably, ATGL is a rate limiting lipolytic enzyme in mammals, which initiates hydrolysis of triglyceride and provides diacylglycerol and fatty acids. Hormone painful and sensitive lipase is yet another important lipolytic enzyme that exhibits Chromoblastomycosis higher substrate affinity for diacylglycerol to make monoacylglycerol. Both enzymes are regulated by cAMP mediated phosphorylation of perilipin. ATGL expression is regulated by FoxO1 that is a school of forkhead proteins. FoxO1 translocation may be stimulated by deprivation of nutrients from the cytosol to nuclei. FoxO1 might bind to the promoter region of the ATGL gene and promotes its transcription. In our review, we demonstrated that fenofibrate improved ACC and AMPK phosphorylation and increased fatty acid b oxidation in C2C12 myotubes. We provided the data that fenofibrate caused ATGL expression was mediated via an PPARa/ AMPK/FoxO1/ATGL route. Dulbeccos modified Eagles medium, fetal calf serum, glutamine, gentamycin, penicillin, and streptomycin were purchased from Life Technologies. 5Aminoimidazole 4 carboxyamide ribonucleoside MAPK pathway cancer and antibodies specific for AMPK, phosphorThr79 ACC, phosphor Thr172 AMPK, ATGL, phospho Ser256 FoxO1, and FoxO1, were acquired from Cell Signaling Technology. Antibodies particular for sterol regulatory element binding protein, a, and carnitine palmitoyltransferase 1 were ordered from Santa Cruz Biotechnology. Antibodies unique for fatty acid synthase and glyceraldehyde 3 phosphate dehydrogenase were obtained from Gene Tex. A monoclonal antibody against RNA polymerase II was from Millipore.