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M J F Newson, G R Pope, E M Roberts, S J Lolait, and A-M O'Carroll

multiple homeostatic perturbations. These include regulation of fluid ( O'Carroll & Lolait 2003 ) and cardiovascular homeostasis ( Ishida et al . 2004 ), the stress response ( O'Carroll et al . 2003 ), food intake ( Taheri et al . 2002 ), gastric cell

Open access

Saadia Basharat, Jennifer A Parker, Kevin G Murphy, Stephen R Bloom, Julia C Buckingham, and Christopher D John

inhibitory role in the regulation of the HPA axis ( Maffei et al . 1995 ). Leptin administration blunts the restraint stress-induced activation of the HPA axis in mice ( Heiman et al . 1997 ) and can directly inhibit ACTH-stimulated cortisol

Open access

R Prasad, J C Kowalczyk, E Meimaridou, H L Storr, and L A Metherell

, differentiation, apoptosis, immune regulation and cellular adaptation to stress ( Ray et al . 2012 , Sena & Chandel 2012 ). A critical balance in redox status needs to be maintained and this is achieved by numerous interacting antioxidant pathways. Oxidative

Open access

Ying Sze, Joana Fernandes, Zofia M Kołodziejczyk, and Paula J Brunton

Introduction Stress experienced during pregnancy has detrimental effects on the offspring across the life course, beginning during fetal development, persisting through the postnatal period and into adulthood ( Glover et al. 2018 ). This

Open access

Bernadette M Trojanowski, Heba H Salem, Heike Neubauer, Eric Simon, Martin Wagner, Rajkumar Dorajoo, Bernhard O Boehm, Leticia Labriola, Thomas Wirth, and Bernd Baumann

early diabetes onset in MODY4 mutation carriers ( Fajans et al. 2010 ). In this condition β-cells are stressed and forced to compensate the increased insulin demand ( Ferrannini et al. 2004 ). Thus, the occurrence of any additional β-cell stress

Open access

Joachim M Weitzel, Torsten Viergutz, Dirk Albrecht, Rupert Bruckmaier, Marion Schmicke, Armin Tuchscherer, Franziska Koch, and Björn Kuhla

the summer period induce metabolic heat stress, which has adverse effects on milk production, reproductive performance and animal welfare issues, among others. Counterregulatory mechanisms generally include an increased sweating rate, increased water

Open access

David O'Regan, Christopher J Kenyon, Jonathan R Seckl, and Megan C Holmes

excess glucocorticoids via maternal stress, inhibition of placental 11β-hydroxysteroid dehydrogenase type 2, the normal ‘barrier’ to maternal glucocorticoids, or its bypass with non-substrate synthetic glucocorticoids, such as dexamethasone (DEX

Open access

Miroslav Adzic, Jelena Djordjevic, Ana Djordjevic, Ana Niciforovic, Constantinos Demonacos, Marija Radojcic, and Marija Krstic-Demonacos

Introduction Response to neuroendocrine stress begins with the activation of the hypothalamic–pituitary–adrenal (HPA) axis leading to the increase in stress hormones glucocorticoids (GCs). These hormones mediate adaptation to stress and also

Open access

Xuefeng Yang, Shuang Mei, Haihua Gu, Huailan Guo, Longying Zha, Junwei Cai, Xuefeng Li, Zhenqi Liu, and Wenhong Cao

. 2009 ). In other words, insulin resistance/hyperinsulinemia is a precursor of T2DM. It is still highly debatable as to how nutrients cause insulin resistance/hyperinsulinemia and then T2DM. Inflammation, endoplasmic reticulum stress, and mitochondrion

Open access

Dawn E W Livingstone, Emma M Di Rollo, Chenjing Yang, Lucy E Codrington, John A Mathews, Madina Kara, Katherine A Hughes, Christopher J Kenyon, Brian R Walker, and Ruth Andrew

Introduction Activation of the hypothalamic–pituitary–adrenal (HPA) axis is a vital component of the stress response, driving production of glucocorticoid hormones (cortisol in humans, corticosterone in rodents) that mediate essential adaptations of