title: Pollen Typhae total flavone improves insulin-induced glucose uptake             through the β-arrestin-2-mediated signaling in C2C12 myotubes.
abstract: Defects in insulin-stimulated glucose uptake in skeletal muscle result from             the dysfunction of insulin signaling including the phosphatidylinositol-3 kinase             (PI3K) pathway and a novel β-arrestin-2-mediated signaling, which leads to insulin             resistance (IR). Pollen Typhae, a Chinese herb, has been used for thousands of             years in traditional Chinese medicine, and has the potential to inhibit the development             of IR. We have previously reported that Pollen Typhae total flavone (PTF), the             extract from Pollen Typhae, ameliorates high-glucose- and high-insulin-induced             impairment of glucose uptake in 3T3-L1 adipocytes, but the mechanisms remain unclear.             The objective of this study was to investigate the effects of PTF on glucose uptake,             and to explore the underlying mechanisms in C2C12 myotubes. PTF improved insulin-stimulated             glucose uptake in a dose- and time-dependent manner in C2C12 myotubes, and prevented             palmitate-induced IR. Furthermore, PTF enhanced the basal gene expression of Src             and Akt2, elevated the protein expression of β-arrestin-2, Src and Akt, increased             the phosphorylation of insulin receptor-β at Tyr1150/1151 and Akt at Thr308/Ser473             in an insulin-dependent manner, but had no effects on the protein expression of             PI3K-p85 or the activity of PI3K. Inhibition of Src but not PI3K restrained PTF-induced             phosphorylation of Akt and glucose uptake. Our findings indicate that PTF improves             insulin-induced glucose uptake via the β-arrestin-2-mediated signaling in C2C12             myotubes.
authors: Institute of Chinese Integrative Medicine, Huashan Hospital, Fudan University, Shanghai, PR China.
authors: Xiao-Tao
authors: XT
authors: Feng
authors: Tian-Zhan
authors: TZ
authors: Wang
authors: Yi
authors: Y
authors: Chen
authors: Ji-Bo
authors: JB
authors: Liu
authors: Yi
authors: Y
authors: Liu
authors: Wen-Jian
authors: WJ
authors: Wang
mesh_terms: D000818:Animals; D019390:Arrestins / Q000235:genetics / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000302:isolation & purification / Q000494:pharmacology*; D047309:Flavones / Q000302:isolation & purification / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D019684:Magnoliopsida / Q000737:chemistry*; D051379:Mice; D018485:Muscle Fibers, Skeletal / Q000187:drug effects* / Q000378:metabolism; D010168:Palmitates / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D011058:Pollen / Q000737:chemistry; D015398:Signal Transduction / Q000187:drug effects; D000071560:beta-Arrestin 2; D000071557:beta-Arrestins
chemical_list: C000605258:Arrb2 protein, mouse; D019390:Arrestins; D004365:Drugs, Chinese Herbal; D047309:Flavones; D007328:Insulin; D010168:Palmitates; D000071560:beta-Arrestin 2; D000071557:beta-Arrestins; D019869:Phosphatidylinositol 3-Kinases; D005947:Glucose