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Department of Internal Medicine, Department of Oncological Endocrinology, Burnett School of Biomedical Sciences, Institute of Human Genetics, Geriatrics Research, Southern Illinois University School of Medicine, 801 North Rutledge Street, Room 4389, Springfield, Illinois 62794-9628, USA
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Department of Internal Medicine, Department of Oncological Endocrinology, Burnett School of Biomedical Sciences, Institute of Human Genetics, Geriatrics Research, Southern Illinois University School of Medicine, 801 North Rutledge Street, Room 4389, Springfield, Illinois 62794-9628, USA
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cardiovascular events ( Lincoff et al . 2007 ). The aim of the study was to analyze the effects of PIO on the insulin-signaling pathway (hepatic levels of insulin receptor (IR), insulin receptor substrate-1 (IRS1) – total and phosphorylated at a serine(307
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Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
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Department of Biochemistry and Molecular Biology, Institute of Human–Environment Interface Biology, Department of Rehabilitation Medicine, Seoul National University College of Medicine, 103 Daehak‐ro, Jongno‐Gu, Seoul 110‐799, Korea
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hypertriglyceridemia ( Gazzerro et al . 2010 ). Moreover, we have demonstrated that the level of CAV1 in skeletal muscle is related to insulin sensitivity in vitro and in vivo ( Oh et al . 2008 ), indicating that CAV1 may regulate insulin signaling. Notably, Cav
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Department of Social and Administrative Sciences, MCPHS University, Boston, Massachusetts, USA
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School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil
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& Kahn 1994 , Cheatham & Kahn 1995 , Virkamaki et al . 1999 ). A growing body of evidence suggests that the phosphorylation of IRS1 at serine 307 is directly linked to the molecular mechanism responsible of the impairment of insulin signaling pathway
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using a glucometer before (0) and after glucose or insulin injection at 5, 10, 15, 30, 60, 90, and 120 min. The glucose area under curve (AUC) for the GTT and ITT was calculated using GraphPad Prism software. To assess insulin signaling in liver and
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kinase 1 (Pak1; Mao et al . 2008 ), in a PI3K-independent manner. This study was conducted to gain further insight into PI3K-induced Akt activation in the insulin signal transduction pathway. To address this, we monitored GLUT4 mobilizations, measured
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, kidney, muscle and adipose tissues, a broad tissue distribution that is characteristic of other FoxO isoforms in mammals ( Kim et al. 2011 ). Recent studies indicate that FoxO6 plays important roles in integrating insulin signaling to glucose and lipid
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Introduction Insulin signaling is the principal pathway that regulates glucose homeostasis of the body. Insulin binds to insulin receptor (IR) and initiates a complex signaling cascade, leading to glucose transporter type 4 (GLUT4
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metabolic action ( Rincon et al. 1996 , Diamanti-Kandarakis & Dunaif 2012 ). It has been proposed that insulin resistance is caused by a post-binding defect in the insulin signaling pathway and/or related to mutations in the insulin receptor ( IR ) gene
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-dependent degradation of β-catenin ( Yi et al . 2008 ). Furthermore, in human hepatocytes, granulosa cells, and C2C12 myotubes, metformin quickly leads to insulin receptor phosphorylation and enhances insulin signaling, e.g., phosphoinositide 3 kinase (PI3K), both in
Medical College, Nantong University, Nantong, Jiangsu Province, China
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Medical College, Nantong University, Nantong, Jiangsu Province, China
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Medical College, Nantong University, Nantong, Jiangsu Province, China
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deletion of BMP7 receptor type 1A in adipose tissue attenuates age-related onset of insulin resistance ( Schulz et al. 2016 ). Thus, it is still unclear whether and how BMP7 regulates insulin signal transduction in the liver. In this study, we increased