title: Effects of Icariin on insulin resistance via the activation of AMPK pathway in C2C12 mouse muscle cells.
abstract: Insulin resistance in skeletal muscle is a major risk factor for the development of type 2 diabetes (T2D). In this study, we investigated the effect of icariin on insulin resistance in C2C12 mouse skeletal muscle cells. C2C12 myoblasts were differentiated into myotubes for five days, then treated with icariin (50 and 100µM) or metformin (1mM) in the presence of 100nM insulin for 24h. Adiponectin production was measured in culture media by ELISA, and AMP-activated protein kinase (AMPK)/insulin signaling pathway activation was assessed by the western blot analysis. Icariin significantly increased adiponectin production in C2C12 myotubes. Moreover, icariin markedly promoted the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC). Icariin up-regulated the expression of phosphatidylinositol 3-kinase (PI3K) and the phosphorylation of insulin receptor substrate-1 (IRS-1) in C2C12 myotubes. These results suggest that icariin has therapeutic potential for the treatment of T2D via the regulation of insulin resistance in skeletal muscle.
authors.affiliation: Korean Medicine R&D Center, Dongguk University, Gyeongju 780-714, Republic of Korea. Electronic address: hanyk1028@hanmail.net.
authors.forename: Yunkyung
authors.initials: Y
authors.lastname: Han
authors.affiliation: Korean Medicine R&D Center, Dongguk University, Gyeongju 780-714, Republic of Korea; Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 780-714, Republic of Korea. Electronic address: tenzing2@hanmail.net.
authors.forename: Hyo Won
authors.initials: HW
authors.lastname: Jung
authors.affiliation: Korean Medicine R&D Center, Dongguk University, Gyeongju 780-714, Republic of Korea; Department of Herbology, College of Korean Medicine, Dongguk University, Gyeongju 780-714, Republic of Korea. Electronic address: yongki@dongguk.ac.kr.
authors.forename: Yong-Ki
authors.initials: YK
authors.lastname: Park
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D052242:Adiponectin / Q000378:metabolism*; D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D005419:Flavonoids / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007333:Insulin Resistance; D008687:Metformin / Q000494:pharmacology; D051379:Mice; D018485:Muscle Fibers, Skeletal / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D058539:Phosphatidylinositol 3-Kinase / Q000096:biosynthesis; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D052242:Adiponectin; D005419:Flavonoids; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D008687:Metformin; D058539:Phosphatidylinositol 3-Kinase; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase; C056599:icariin
keywords: AMPK pathway; C2C12 cells; Icariin; Insulin resistance; Skeletal muscle; Type 2 diabetes