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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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Department of Pharmaceutical Sciences, University of Salerno, ‘Federico II’, Naples, Italy
Department of Pathology and Animal Health, University of Naples ‘Federico II’, Naples, Italy
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). Discussion During pregnancy, physiological adaptation in the nutritional and hormonal setting is necessary for fetal growth and maternal well-being. When pathological conditions, such as obesity or hypertension, occur, further modifications are needed
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-dependent stress response involving DNA-PK occurs in hypoxic cells and contributes to cellular adaptation to hypoxia . Journal of Cell Science 124 1943 – 1951 . ( doi:10.1242/jcs.078030 ) Branco MR Oda M Reik W 2008 Safeguarding parental
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Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
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I Mogilner J Shamir R Shehadeh N Bejar J Hirsh M Coran AG 2005 Effect of subcutaneous insulin on intestinal adaptation in a rat model of short bowel syndrome . Pediatric Surgery International 21 132 – 137 . ( doi:10.1007/s00383
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Kloet ER Joëls M Holsboer F 2005 Stress and the brain: from adaptation to disease . Nature Reviews. Neuroscience 6 463 – 475 . Koletsky S Shook P Rivera-Velez J 1972 Absence of a hyperactive renal humoral pressor system in spontaneously
IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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et al. 1987 , Manzon 2002 ) or growth hormone (i.e. the gh/igfI axis; Sakamoto et al. 1993 , McCormick 2001 ) in the adaptation to gradual or rapid salinity changes; also in the ontogenetic acquisition of salinity tolerance, these hormones play
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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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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.