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Giuseppina Mattace Raso Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Giuseppe Bianco Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Anna Iacono Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Emanuela Esposito Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Giuseppina Autore Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Maria Carmela Ferrante Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Antonio Calignano Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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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Rosaria Meli Department of Experimental Pharmacology, University of Naples, ‘Federico II’, via D. Montesano, 49-80131 Naples, Italy
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

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0159
Volume/Issue:
Volume 194: Issue 3
Free access
Kimberley C W Wang Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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Kimberley J Botting Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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Song Zhang Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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I Caroline McMillen Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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Doug A Brooks Mechanisms in Cell Biology and Disease Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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Janna L Morrison Early Origins of Adult Health Research Group, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia

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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

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-17-0039
Volume/Issue:
Volume 233: Issue 2
Free access
Tatiana Dorfman 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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Yulia Pollak 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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Rima Sohotnik 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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Arnold G Coran 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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Jacob Bejar 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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Igor Sukhotnik 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
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

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0725
Volume/Issue:
Volume 226: Issue 3
Free access
A L Markel
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O E Redina
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M A Gilinsky Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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G M Dymshits Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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E V Kalashnikova Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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Yu V Khvorostova Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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L A Fedoseeva Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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G S Jacobson Laboratory of Evolutionary Genetics, Laboratory of Adaptation Processes Regulation, Laboratory of Genome Structure, Laboratory of Pathophysiology, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 10 Lavrentieva Avenue, 630090 Novosibirsk, Russia

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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

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0254
Volume/Issue:
Volume 195: Issue 3
Free access
Stamatis Varsamos Adaptation Ecophysiologique et Ontogenèse, UMR 5171, GPIA, Université Montpellier II, Place Eugène Bataillon, CC092, 34095 Montpellier Cedex 05, France
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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Benoît Xuereb Adaptation Ecophysiologique et Ontogenèse, UMR 5171, GPIA, Université Montpellier II, Place Eugène Bataillon, CC092, 34095 Montpellier Cedex 05, France
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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Thérèse Commes Adaptation Ecophysiologique et Ontogenèse, UMR 5171, GPIA, Université Montpellier II, Place Eugène Bataillon, CC092, 34095 Montpellier Cedex 05, France
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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Gert Flik Adaptation Ecophysiologique et Ontogenèse, UMR 5171, GPIA, Université Montpellier II, Place Eugène Bataillon, CC092, 34095 Montpellier Cedex 05, France
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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Céline Spanings-Pierrot Adaptation Ecophysiologique et Ontogenèse, UMR 5171, GPIA, Université Montpellier II, Place Eugène Bataillon, CC092, 34095 Montpellier Cedex 05, France
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

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06847
Volume/Issue:
Volume 191: Issue 2
Free access
Charles A Ducsay
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Dean A Myers Center for Perinatal Biology, Department of Obstetrics and Gynecology, Loma Linda University School of Medicine, Loma Linda, California 92350, USA

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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.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0034
Volume/Issue:
Volume 210: Issue 3
Free access
H Yokoi
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H Nagasaki
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K Tachikawa
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H Arima
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T Murase
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Y Miura
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M Hirabayashi
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Y Oiso
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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.

Article Type:
Other
DOI:
https://doi.org/10.1677/joe.0.1730023
Volume/Issue:
Volume 173: Issue 1
Free access
Erica Yeo Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada

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Patricia L Brubaker Department of Physiology, University of Toronto, Toronto, ON, Canada
Department of Medicine, University of Toronto, Toronto, ON, Canada

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Deborah M Sloboda Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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

Article Type:
Review Article
Collections:
Gut microbiome special collection
DOI:
https://doi.org/10.1530/JOE-21-0354
Volume/Issue:
Volume 253: Issue 1
Open access
D S Boeldt Perinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin‐Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA

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F X Yi Perinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin‐Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA

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I M Bird Perinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin‐Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA

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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

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0053
Volume/Issue:
Volume 210: Issue 3
Free access
Hidetada Ogata 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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Yusuke Seino 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
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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Norio Harada 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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Atsushi Iida 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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Kazuyo Suzuki 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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Takako Izumoto 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
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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Kota Ishikawa 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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Eita Uenishi 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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Nobuaki Ozaki 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
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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Yoshitaka Hayashi 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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Takashi Miki 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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Nobuya Inagaki 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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Shin Tsunekawa 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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Yoji Hamada 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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Susumu Seino 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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Yutaka Oiso 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.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0161
Volume/Issue:
Volume 222: Issue 2
Free access