, genetically fat or lean chickens, or exogenous insulin challenge ( Dupont et al . 1998 a , b , c , 1999 , 2004 )). In contrast, these signaling steps (with the exception of Shc) were not altered in leg muscles by the various experimental conditions. This
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Joëlle Dupont, Sophie Tesseraud, Michel Derouet, Anne Collin, Nicole Rideau, Sabine Crochet, Estelle Godet, Estelle Cailleau-Audouin, Sonia Métayer-Coustard, Michel J Duclos, Christian Gespach, Tom E Porter, Larry A Cogburn, and Jean Simon
María Florencia Heber, Silvana Rocío Ferreira, Giselle Adriana Abruzzese, Raíces Trinidad, Omar P Pignataro, Margarita Vega, and Alicia B Motta
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
Tsun-Jui Liu, Hui-Chin Lai, Chih-Tai Ting, and Ping H Wang
Introduction Insulin-like growth factor-I (IGF-I) and insulin are part of the complex regulatory mechanisms that help to maintain normal myocardial function ( Abel 2004 , Saetrum & Wang 2005 ). Signaling pathways of IGF-I receptor
M Schütt, J Zhou, M Meier, and H H Klein
insulin signaling at the level of insulin-receptor substrate (IRS)-1 phosphorylation ( Schütt et al. 2000 , Cammalleri & Germinario 2003 ), association of the p85 subunit of phosphatidylinositol 3-kinase (PI3-kinase; Schütt et al. 2000 ) and/or Thr
Hong Ma, Jin Yuan, Jinyu Ma, Jie Ding, Weiwei Lin, Xinlei Wang, Mingliang Zhang, Yi Sun, Runze Wu, Chun Liu, Cheng Sun, and Yunjuan Gu
(IR) ( Dulloo & Montani 2012 ). IR is a hallmark of T2D, in which insulin at normal physiological concentrations fails to effectively activate its downstream signal transduction in the skeletal muscle, liver and adipose tissue ( Hartstra et al. 2015
Cathy A Guo and Shaodong Guo
cardiomyopathy. In this review, we discuss the mechanisms of insulin in governing cardiac energetics, and update on how insulin resistance promotes cellular dysfunction at the molecular level with interacting signaling cascade involving in IRS-1, -2 and Foxo1
Sojin Lee and H Henry Dong
attenuated insulin-like signaling or increased oxidative stress, promotes anti-oxidative function, contributing to the lifespan extension in Caenorhabditis elegans ( Lee et al. 2003 ). Likewise, the FoxO1 ortholog dFoxO signaling through insulin
Jie Xu, Shaonin Ji, Derwei Y Venable, John L Franklin, and Joseph L Messina
investigated the effects of prolonged insulin on GH signaling via the other two STATs (STAT3 and STAT1) in rat H4IIE hepatoma cells. We found that prolonged insulin pretreatment inhibited not only GH-induced tyrosine phosphorylation (PY) of STAT3 and STAT1 but
Adam Gesing, Andrzej Bartke, and Michal M Masternak
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
Shaodong Guo
molecular, biochemical, and physiological levels. Part 1: molecular basis of insulin signaling Insulin and signal transduction studies have resulted in breakthroughs in the area of diabetes and biomedical research. Innovative attempts at insulin purification
