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Elena Conte, Adele Romano, Michela De Bellis, Marialuisa de Ceglia, Maria Rosaria Carratù, Silvana Gaetani, Fatima Maqoud, Domenico Tricarico, and Claudia Camerino

-Oxtr vector ( Kasahara et al. 2013 ). We previously demonstrated that Oxt regulates the response to cold stress (CS) in mice through a feed-forward loop in the brain ( Camerino et al. 2017 ). Gene expression analysis shows that mRNA levels of Oxtr are

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Ernest Sargsyan, Henrik Ortsäter, Kristofer Thorn, and Peter Bergsten

exerts its positive effect have been investigated. In the present study, we wanted to explore whether induction of endoplasmic reticulum (ER) stress ( Wu & Kaufman 2006 ), which has been observed in β-cells exposed to elevated levels of glucose and fatty

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The effects of stress, induced by overcrowding adult male mice, have been examined in relation to adrenal size and to epidermal mitotic activity. After 3 weeks the size (expressed as the maximum sectional area) of the adrenal medulla of the crowded mice increased by about 80 %, while that of the cortex increased by about 30 %. Simultaneously, the epidermal mitotic rate fell by about 60 %.

The effects of the adrenal hormones on epidermal mitosis were next studied. It was found that adrenaline has a powerful antimitotic action both in vivo and in vitro, and that the same is true of the glucocorticoid hormone, 11-dehydro-17-hydroxycorticosterone-21-acetate (cortisone).

It is suggested that the antimitotic effects of stress may be due to a high rate of secretion of either, or both, these adrenal hormones, and that these substances act through some interference in carbohydrate metabolism. When energy production is inhibited, it is known that, while no new epidermal mitosis can develop, there is no impediment to the completion of any division already in progress, and this is the precise pattern of inhibition produced by both adrenaline and cortisone.

Evidence is reviewed to suggest that the antimitotic action of these hormones may be related to an inhibition of hexokinase. Adrenaline is not known to affect this enzyme, but it is rapidly oxidized to adrenochrome which does. It is shown that adrenochrome has a powerful antimitotic action.

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Nicholas J Bernier, Sarah L Alderman, and Erin N Bristow

Introduction The corticotropin-releasing factor (CRF) system is a key player in the coordination and regulation of the vertebrate stress response. In teleosts, as in amphibians and mammals, the CRF system is composed of four paralogous lineages of

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Yoon Sin Oh, Youn-Jung Lee, Yup Kang, Jaeseok Han, Oh-Kyung Lim, and Hee-Sook Jun

. 2004 ). Several potential mechanisms underlying β-cell dysfunction caused by glucolipotoxicity have been suggested, including reactive oxygen species-mediated oxidative stress, inflammatory signals, lipid intermediates, and ER stress ( Donath et al

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Yolanda Diz-Chaves, Manuel Gil-Lozano, Laura Toba, Juan Fandiño, Hugo Ogando, Lucas C González-Matías, and Federico Mallo

Introduction The stress indices in Western societies are correlated with the increasing rates of obesity and metabolic syndrome. Recent data indicate that chronic stress, associated with mild hypercortisolaemia and prolonged sympathetic

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Xiaoyi Ma, Fei Gao, Qi Chen, Xiuping Xuan, Ying Wang, Hongjun Deng, Fengying Yang, and Li Yuan

responses and oxidative stress ( Shi et al . 2018 ), thus positively regulating beta-cell function and insulin release ( Yuan et al . 2014 , Brar et al . 2017 ). In our previous studies, A1–7 was found to improve vascular endothelial growth factor (VEGF

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C Doyon, V L Trudeau, and T W Moon

Introduction The primary stress response involves the activation of hypothalamic neurons producing corticotropin-releasing factor (CRF), an initial step in the cascade that leads to the synthesis and release of glucocorticoids

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S Hesketh, D S Jessop, S Hogg, and M S Harbuz

Introduction The hypothalamic–pituitary–adrenal (HPA) axis serves as a neuroendocrine stress response system, which has an important role in the maintenance of homeostatsis ( Buckingham et al. 1997 ). Stimulation of the HPA axis

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Eleftheria Diakogiannaki, Hannah J Welters, and Noel G Morgan

that the lipotoxic demise of the pancreatic β-cells may be related to a process of endoplasmic reticulum (ER) stress ( Kharroubi et al . 2004 , Karaskov et al . 2006 , Eizirik et al . 2008 ) and that this culminates in enhanced cell loss by