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revealed that the largest increases in the abundance of polysomal mRNAs encoded proteins associated with oxidative stress, indicating that the expression of these proteins is up-regulated in response to high glucose concentration (Table 2 ). These included
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Department of Endocrinology, St Bartholomew's Hospital, London ec1a 7be received 16 February 1988 While stress and opiate alkaloids such as morphine have both been with us for millenia, the relationship between the two has remained obstinately enigmatic. The discovery of the endogenous opioid peptides some 13 years ago suggested that we might at last have found the key, but the partners to the relationship, while clearly well disposed to each other, persist in avoiding legal wedlock. Can we not find grounds at least for a prolonged engagement between stress and the opioids in current neuroendocrinology?
Introduction
Circulating opioid peptides
Endorphins
Measurement of circulating opioid peptides has certainly not been encouraging, following the initial euphoria in discovering that certain opioids were indeed present in the peripheral circulation. In man, β-lipotrophin (β-LPH) is co-released with adrenocorticotrophin (ACTH) after cleavage from pro-opiomelanocortin in the corticotrophs of the anterior pituitary,
Graduate School of Peking Union Medical College, Institute of Clinical Medical Sciences, Department of Cell Physiology and Metabolism, Beijing 100730, People's Republic of China
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Introduction Progressive β-cell failure is the precipitating factor for the transition from the insulin-resistant state to overt type 2 diabetes ( Muoio & Newgard 2008 ). Hyperglycemia and oestrogen receptor (ER) stress have been suggested as
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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
Lee Gil Ya Cancer and Diabetes Institute, Department of Endocrinology and Metabolism, Howard Hughes Medical Institute, Gachon Medical Research Institute, Department of Rehabilitation Medicine, College of Pharmacy, Gachon University, 7-45 Songdo‐dong, Yeonsu‐ku, Incheon, Korea
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Lee Gil Ya Cancer and Diabetes Institute, Department of Endocrinology and Metabolism, Howard Hughes Medical Institute, Gachon Medical Research Institute, Department of Rehabilitation Medicine, College of Pharmacy, Gachon University, 7-45 Songdo‐dong, Yeonsu‐ku, Incheon, Korea
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. 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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Department of Physiology and Pharmacology ‘V. Erspamer’, SAPIENZA University, Rome, Italy
Department of Biomedical Sciences and Human Oncology (Section of Pharmacology), School of Medicine, University of Bari, Bari, Italy
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-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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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
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain
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Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain
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Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain
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Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain
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Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain
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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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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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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
