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Linda Ahlkvist Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Bilal Omar Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Anders Valeur Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Keld Fosgerau Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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Bo Ahrén Department of Clinical Sciences, Zealand Pharma A/S, Biomedical Center, Lund University, SE 22184 Lund, Sweden

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tolerance test (IVGTT) was performed where the mice were injected with glucose (0.35 g/kg, Sigma) in a tail vein with or without glucagon-like peptide 1 (GLP1) (3 nmol/kg, Sigma). Blood samples were collected at different time points into heparinized tubes

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0371
Volume/Issue:
Volume 228: Issue 3
Free access
Shin-ya Ueda Department of Sports Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

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Takahiro Yoshikawa Department of Sports Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

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Yoshihiro Katsura Department of Sports Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

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Tatsuya Usui Department of Sports Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

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Shigeo Fujimoto Department of Sports Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

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number of gastrointestinal hormones, such as peptide YY (PYY) and glucagon-like peptide-1 (GLP-1 or GCG as listed in the HUGO Database; Huda et al . 2006 , Näslund & Hellström 2007 , Wren & Bloom 2007 ). PYY is recognized as a satiety factor

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0190
Volume/Issue:
Volume 203: Issue 3
Free access
Jung-Hoon Kang Internal Medicine, Department of Internal Medicine, Departments of

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Seo-Yoon Chang Internal Medicine, Department of Internal Medicine, Departments of

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Hyun-Jong Jang Internal Medicine, Department of Internal Medicine, Departments of

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Dong-Bin Kim Internal Medicine, Department of Internal Medicine, Departments of

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Gyeong Ryul Ryu Internal Medicine, Department of Internal Medicine, Departments of

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Seung Hyun Ko Internal Medicine, Department of Internal Medicine, Departments of

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In-Kyung Jeong Internal Medicine, Department of Internal Medicine, Departments of

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Yang-Hyeok Jo Internal Medicine, Department of Internal Medicine, Departments of

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Myung-Jun Kim Internal Medicine, Department of Internal Medicine, Departments of

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or reduce iNOS expression may be necessary for the prevention or inhibition of β-cell damage. Glucagon-like peptide-1 (GLP-1) and its potent agonist exendin-4 (EX-4) have received great attention because of their insulinotropic and β

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0507
Volume/Issue:
Volume 202: Issue 1
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Ashley I Taylor SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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Nigel Irwin SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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Aine M McKillop SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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Steven Patterson SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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Peter R Flatt SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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Victor A Gault SAAD Centre for Pharmacy and Diabetes, School of Biomedical Sciences Research Institute, University of Ulster, Coleraine BT52 1SA, UK

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has examined the plasma stability and satiety effects of xenin, and further characterised the glucose-lowering and insulinotropic effects of xenin both alongside GIP, glucagon-like peptide-1 (GLP1) and neurotensin. Materials and Methods Degradation of

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-10-0085
Volume/Issue:
Volume 207: Issue 1
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Bethany P Cummings Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA
Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Andrew A Bremer Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Timothy J Kieffer Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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David D'Alessio Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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Peter J Havel Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA
Department of Molecular Biosciences, Department of Nutrition, Department of Pediatrics, Department of Physiology, Division of Endocrinology, School of Veterinary Medicine, University of California Davis, One Shields Avenue, Davis, California 95616, USA

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hypothesized that dexamethasone may enhance postprandial insulin secretion by increasing meal-stimulated incretin hormone secretion and/or by increasing parasympathetic input to the pancreas. The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0459
Volume/Issue:
Volume 216: Issue 2
Free access
Catia Martins School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK
Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London W12 ONN, UK

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Linda M Morgan School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK
Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London W12 ONN, UK

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Stephen R Bloom School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK
Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London W12 ONN, UK

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M Denise Robertson School of Biomedical and Molecular Sciences, University of Surrey, Guildford GU2 7XH, UK
Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London W12 ONN, UK

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), peptide YY (PYY), glucagon-like peptide-1 (GLP-1) and pancreatic polypeptide (PP) ( Blundell 1991 , King et al. 1997 b ). These metabolic and endocrine signals are then received and processed by specific areas in the hypothalamus and brainstem

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-06-0030
Volume/Issue:
Volume 193: Issue 2
Free access
Carmen Sanz Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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Isabel Roncero Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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Patricia Vázquez Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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M Angeles Navas Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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Enrique Blázquez Department of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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glucose concentrations and peptides on GK gene promoter expression was tested in transiently transfected GT1-7 cells. Neither different glucose concentrations (2.8, 5.5, 10, or 20 mM) nor leptin (LEP), glucagon-like peptide 1 (GLP-1) or neuropeptide Y

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-06-0146
Volume/Issue:
Volume 193: Issue 2
Free access
Helena A Walz Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Linda Härndahl Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Nils Wierup Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Emilia Zmuda-Trzebiatowska Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Fredrik Svennelid Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Vincent C Manganiello Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Thorkil Ploug Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Frank Sundler Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Eva Degerman Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Bo Ahrén Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Lena Stenson Holst Department of Experimental Medical Science, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden

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Introduction Intracellular cAMP is crucial for pancreatic β-cell function. Insulin secretion stimulated by glucagon and incretin hormones, e.g. glucagon-like peptide-1 (GLP-1), is exerted via increased cAMP ( Gromada et al. 1998

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06522
Volume/Issue:
Volume 189: Issue 3
Free access
A Alidibbiat
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C E Marriott Diabetes Research Group, School of Pharmacy and Biomolecular Sciences, Department of Diabetes, Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK

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K T Scougall
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S C Campbell
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G C Huang Diabetes Research Group, School of Pharmacy and Biomolecular Sciences, Department of Diabetes, Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK

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W M Macfarlane Diabetes Research Group, School of Pharmacy and Biomolecular Sciences, Department of Diabetes, Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK

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J A M Shaw
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–Aldrich; glucagon-like peptide 1 (7–36) (GLP1) from Bachem (Merseyside, UK) and Betacellulin (BTC) from R&D Systems (Oxon, UK). M-MLV reverse transcriptase, oligo dTs, dNTPs and RNase-free DNase were from Promega; Red Taq polymerase from Sigma–Aldrich and Matrigel

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0397
Volume/Issue:
Volume 196: Issue 1
Free access
Jordan S F Chan Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Amanda A Greenwell Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Christina T Saed Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Magnus J Stenlund Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Indiresh A Mangra-Bala Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Seyed Amirhossein Tabatabaei Dakhili Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Kunyan Yang Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Sally R Ferrari Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Farah Eaton Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Keshav Gopal Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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John R Ussher Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada
Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada
Cardiovascular Research Institute, University of Alberta, Edmonton, Alberta, Canada

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Introduction Glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) agonists are glucose-lowering agents for type 2 diabetes (T2D) that promote insulin secretion ( Campbell & Drucker 2013 ). The clinical use of GLP-1R agonists is expanding due to

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-24-0032
Volume/Issue:
Volume 262: Issue 2
Restricted access