expression is independent of circulating TH concentration ( Zoeller et al . 1990 ) or of nutritional status ( Jaimes-Hoy et al . 2008 ), but is inhibited by a previous stress exposure ( Uribe et al . 2011 ) or corticosterone injection ( Sotelo-Rivera et
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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, Rosa-María Uribe, and Jean-Louis Charli
Aowen Zhuang and Josephine M Forbes
develop a detrimental condition referred to as ER stress. The principles of the UPR are now relatively well defined ( Ron & Walter 2007 , Hasnain et al . 2012 , Hetz 2012 ), and the mechanisms of the signal transducers involved in the activation of this
Georgia Balsevich, Andres Uribe, Klaus V Wagner, Jakob Hartmann, Sara Santarelli, Christiana Labermaier, and Mathias V Schmidt
Introduction The global prevalence of obesity is rising ( Yach et al . 2006 ), emphasizing the need to decipher the complex regulatory mechanisms underlying energy balance. Evidence indicates that chronic stress is a risk factor for obesity
Jordan E Hamden, Katherine M Gray, Melody Salehzadeh, and Kiran K Soma
Introduction The effects of early-life stress (ELS) are profound, long lasting, and diverse. ELS impacts growth, metabolism, immunity, brain physiology, and behavior ( Meaney & Plotsky 2000 , Lehmann et al. 2002 , Levine 2002 , Bilbo et
Stephen G Matthews and Patrick O McGowan
maternal stress/anxiety/depression, maternal obesity, maternal glucocorticoid exposure and altered level of maternal care. While early studies in the field were confined to animal models, more recently, they have been extended to include humans. The
Ralf Baumeister, Elke Schaffitzel, and Maren Hertweck
in lipid biosynthesis and storage ( Mak et al. 2006 ), regulatory micro-RNAs ( Mansfield et al. 2004 ), neurotrans-mission, and the control of developmental decisions, stress response, and lifespan ( Lee et al. 2003 , Hamilton et al. 2005
Takahiro Nemoto, Yoshihiko Kakinuma, and Tamotsu Shibasaki
dexamethasone ( Holsboer-Trachsler et al . 1987 , Hoshino et al . 1987 , Vreeburg et al . 2009 , Hempel et al . 2010 ), and abnormal adrenocorticotropin (ACTH) and cortisol responses to corticotropin-releasing factor (CRF) or stress ( Young et al . 2000
Stephen Mandang, Ursula Manuelpillai, and Euan M Wallace
of excessive oxidative stress ( Hubel 1999 , Burton & Jauniaux 2004 , Myatt & Cui 2004 ), thought to result from either hypoxia-reperfusion injury ( Burton & Hung 2003 ) and/or deficient antioxidant defences ( Perkins 2006 ). In turn, increased
R Mastrocola, F Restivo, I Vercellinatto, O Danni, E Brignardello, M Aragno, and G Boccuzzi
intracellular glucose oxidation ( Nishikawa et al. 2000 ), which leads to an increase in reactive species production ( Bonnefont-Rousselot 2002 , Evans et al. 2002 ): in both man and experimentally diabetic rats, oxidative stress seems to play a central
Francesca Spiga, Louise R Harrison, Cliona P MacSweeney, Fiona J Thomson, Mark Craighead, and Stafford L Lightman
of the vasopressin 1b receptor (AVPR1B; Aguilera et al . 1994 ). AVP levels and secretion, as well as AVP mRNA expression within the parvocellular PVN, increase in response to repeated exposure to stressors such as restraint ( de Goeij et al
