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When rainbow trout (Salmo gairdneri) and eels (Anguilla anguilla) were kept in black tanks for 3—4 weeks, their plasma cortisol titres were about fourfold higher than in fish kept in white tanks. In trout, the difference was apparent only under a long photoperiod of 16 h light: 8 h darkness, but in eels the difference was clear under both a long or short photoperiod (9·5 h light: 14·5 h darkness). It is suggested that the increase in plasma cortisol seen in black-adapted fish is dependent on either ACTH or MSH secreted by the pars intermedia melanotrophs. No difference was seen either in the total cortisol-binding capacity of the plasma nor in interrenal histology in trout from black or white backgrounds.
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Nitric oxide (NO) plays a role in a wide range of physiological processes. Aside from its widely studied function in the regulation of vascular function, NO has been shown to impact steroidogenesis in a number of different tissues. The goal of this review is to explore the effects of NO on steroid production and further, to discern its source(s) and mechanism of action. Attention will be given to the regulation of NO synthases in specific endocrine tissues including ovaries, testes, and adrenal glands. The effects of hypoxia on generation of NO and subsequent effects on steroid biosynthesis will also be examined. Finally, a potential model for the interaction of hypoxia on NO synthesis and steroid production is proposed.
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SUMMARY
Large and rapid variations were found in the plasma cortisol levels of housed and cannulated sheep. Adrenaline injected i.v. caused increased plasma levels of cortisol that were proportionate to the dose. This response of cortisol to adrenaline was larger when sheep were newly housed, than when the sheep had been housed and sampled for 2 weeks. Response to adrenocorticotrophin also diminished over 2 weeks. Dexamethasone abolished the response to adrenaline. Tyrosine and DOPA had little effect on cortisol levels, dopamine and noradrenaline had some effect, but none had as great an effect as adrenaline.
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SUMMARY
Sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) activity increased in the urinary bladder of the euryhaline teleost Platichthys stellatus after transfer from sea-water to fresh water. This increase also occurred after injection of prolactin into seawater Platichthys, simulating the results of freshwater transfer. In Kareius bicoloratus, which does not survive transfer to fresh water, prolactin does not increase bladder Na-K-ATPase activity. The differences in response of these two species to prolactin may be related to the degree of their euryhalinity. There may be a relationship between adaptability to fresh water and responsiveness of bladder Na-K-ATPase to prolactin.
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Prolonged exposure of tissues to a receptor agonist often leads to adaptive changes that limit the subsequent responsiveness of the tissue to the same agonist. Recently, we have generated rats transgenic for the metallothionein I-human arginine vasopressin (AVP) fusion gene (Tg), which produced high plasma AVP with relatively preserved renal water excretion, suggesting that there might be adaptive mechanism(s) for maintaining water and electrolyte homeostasis against chronic AVP oversecretion from the earliest stage of life. In this study, to investigate whether down-regulation of AVP V2 receptor (V2R), which could possibly be caused by long-standing high plasma AVP, participates in this adaptive mechanism(s), non-peptidic V2R antagonist OPC31260 was administered to reverse the down-regulation, and water loading was performed after V2R antagonist treatment had been withdrawn. Additionally, to confirm the down-regulation, Northern blotting analysis for V2R mRNA was carried out. Tg rats showed slightly decreased urine volume and water intake with an equivalent plasma [Na(+)] level (Tg 140.4 +/- 0.6 mEq/l; control 139.3 +/- 0.6 mEq/l) under basal conditions. After water loading using a liquid diet containing zinc, which stimulates the promoter region in the transgene, the urine increase showed only limited suppression with a dramatically increased plasma AVP level and mild hyponatremia (135.8 +/- 1.8 mEq/l) in Tg rats. When diet containing OPC31260 had been provided for 4 days until the day before the start of water loading, antidiuresis and hyponatremia (125.4 +/- 1.mEq/l) were significantly potentiated. V2R mRNA expression in kidney was significantly less in Tg rats than in control rats under basal conditions, and this suppression was restored by OPC31260 treatment to levels comparable with those of control rats. These results suggest that long-standing high plasma AVP causes V2R down-regulation, and it may play an important role in the adaptive mechanism(s) for maintaining water and electrolyte homeostasis in chronically AVP-overexpressing rats.
Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
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Department of Medicine, University of Toronto, Toronto, ON, Canada
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Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada
Department of Obstetrics, Gynecology and Pediatrics, McMaster University, Hamilton, ON, Canada
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Introduction To accommodate the dynamic energy demands of pregnancy, while still maintaining metabolic homeostasis, significant alterations to maternal metabolism are required ( Fig. 1 ). Impaired or inappropriate maternal adaptations can
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Introduction: evidence for pregnancy adaptation of cell signaling and associated changes in nitric oxide output Pregnancy-specific programming of endothelial nitric oxide production Nitric oxide (NO) is an important vasodilator produced by vascular
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Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
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Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
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Departments of Endocrinology and Diabetes, Metabolic Medicine, Department of Diabetes, Department of Oral and Maxillofacial Surgery, Research Center of Health, Division of Stress Adaptation and Recognition, Department of Medical Physiology, Division of Molecular and Metabolic Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
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Glucose-dependent insulinotropic polypeptide (GIP), a gut hormone secreted from intestinal K-cells, potentiates insulin secretion. Both K-cells and pancreatic β-cells are glucose-responsive and equipped with a similar glucose-sensing apparatus that includes glucokinase and an ATP-sensitive K+ (KATP) channel comprising KIR6.2 and sulfonylurea receptor 1. In absorptive epithelial cells and enteroendocrine cells, sodium glucose co-transporter 1 (SGLT1) is also known to play an important role in glucose absorption and glucose-induced incretin secretion. However, the glucose-sensing mechanism in K-cells is not fully understood. In this study, we examined the involvement of SGLT1 (SLC5A1) and the KATP channels in glucose sensing in GIP secretion in both normal and streptozotocin-induced diabetic mice. Glimepiride, a sulfonylurea, did not induce GIP secretion and pretreatment with diazoxide, a KATP channel activator, did not affect glucose-induced GIP secretion in the normal state. In mice lacking KATP channels (Kir6.2 −/− mice), glucose-induced GIP secretion was enhanced compared with control (Kir6.2 + / + ) mice, but was completely blocked by the SGLT1 inhibitor phlorizin. In Kir6.2 −/− mice, intestinal glucose absorption through SGLT1 was enhanced compared with that in Kir6.2 + / + mice. On the other hand, glucose-induced GIP secretion was enhanced in the diabetic state in Kir6.2 + / + mice. This GIP secretion was partially blocked by phlorizin, but was completely blocked by pretreatment with diazoxide in addition to phlorizin administration. These results demonstrate that glucose-induced GIP secretion depends primarily on SGLT1 in the normal state, whereas the KATP channel as well as SGLT1 is involved in GIP secretion in the diabetic state in vivo.
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, driven primarily by gestational changes in maternal and placental hormones. These adaptations accommodate the growing conceptus and prepare the mother for parturition and postnatal parenting. Impaired maternal adaptation to pregnancy, particularly from a
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Department of Pediatrics, University of Kansas Medical Center, Kansas City, Kansas, USA
Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, Kansas, USA
Center for Perinatal Research, Children’s Research Institute, Children’s Mercy, Kansas City, Missouri, USA
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, hypertensive disorders, premature birth, cesarean delivery and development of metabolic disorders such as obesity and diabetes later in life ( Vambergue & Fajardy 2011 , Zhu & Zhang 2016 ). GDM is a consequence of unsatisfactory pregnancy-dependent adaptations
