Triglyceride accumulation in skeletal muscles increases in subjects with insulin resistance. The increase of triglyceride accumulation is a direct result decreased mitochondrial fatty acid supplier Capecitabine oxidation in cells. Fenofibrate was proven to avoid the development of diabetes in obese diabetes vulnerable rats, however the system isn’t completely comprehended. The mobile gas gauge, 50 AMP activated protein kinase, a power warning protein, is generally accepted as a target for treating diabetes. Fenofibrate was shown to activate AMPK in human umbilical vein endothelial cells and retinal endothelial cells, but whether fenofibrate regulates lipid k-calorie burning through an AMPK route has not been investigated 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 improves the transportation of fatty acid into mitochondria for fatty acid t oxidation. ATGL, a discovered lipase, is responsible for triglyceride hydrolase activity in cells and is generally accepted as a therapeutic goal for dyslipidemia and fatty liver. Significantly, ATGL is just a rate limiting lipolytic enzyme in animals, which initiates hydrolysis of triglyceride and produces diacylglycerol and essential fatty acids. Hormone sensitive and painful lipase is yet another key lipolytic enzyme that displays Eumycetoma higher substrate affinity for diacylglycerol to make monoacylglycerol. Both enzymes are regulated by cAMP mediated phosphorylation of perilipin. ATGL expression is controlled by FoxO1 that is a type of forkhead proteins. FoxO1 translocation may be stimulated by deprivation of nutrients from the cytosol to nuclei. FoxO1 may bind to the promoter region of the ATGL gene and increases its transcription. In our review, we demonstrated that fenofibrate increased ACC and AMPK phosphorylation and increased fatty acid t oxidation in C2C12 myotubes. We presented the evidence that fenofibrate caused ATGL expression was mediated via an PPARa/ AMPK/FoxO1/ATGL process. Dulbeccos changed Eagles medium, fetal calf serum, glutamine, gentamycin, penicillin, and streptomycin were obtained from Life Technologies. 5Aminoimidazole 4 carboxyamide ribonucleoside order A66 and antibodies specific for AMPK, phosphor Thr172 AMPK, phosphorThr79 ACC, ATGL, phospho Ser256 FoxO1, and FoxO1, were bought from Cell Signaling Technology. Antibodies unique for sterol regulatory element binding protein, a, and carnitine palmitoyltransferase 1 were ordered from Santa Cruz Biotechnology. Antibodies certain for glyceraldehyde 3 phosphate dehydrogenase and fatty acid synthase were obtained from Gene Tex. A monoclonal antibody against RNA polymerase II was from Millipore.