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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Introduction Glucagon and glucagon-like peptide-1 (GLP-1) are processed from the same precursor, proglucagon ( Fig. 1 ), and have opposite effects on glucose homeostasis ( 1 , 2 , 3 ). In the intestine, proglucagon is cleaved by prohormone
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NNF Center for Basic Metabolic Research and Department of Biomedical Sciences, Department of Science, Faculty of Health Science, University of Copenhagen, Blegdamsvej 3B, 12.2, DK‐2200 Copenhagen N, Denmark
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Introduction Glucagon-like peptide 1 (GLP-1) and glucagon arise from differential processing of the glucagon precursor, proglucagon (PG) (1) . Both peptides are important for normal glucose homeostasis, which focused interest on their potential
Department of Endocrinology and Internal Medicine, Novo Nordisk A/S, NNF center for Basic Metabolic Research, Department of Clinical Biochemistry, Department of Clinical Physiology and Molecular Imaging, Department of Clinical Medicine, Aarhus University Hospital, Norrebrogade 44, DK-8000 Aarhus, Denmark
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Department of Endocrinology and Internal Medicine, Novo Nordisk A/S, NNF center for Basic Metabolic Research, Department of Clinical Biochemistry, Department of Clinical Physiology and Molecular Imaging, Department of Clinical Medicine, Aarhus University Hospital, Norrebrogade 44, DK-8000 Aarhus, Denmark
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Introduction Glucagon-like peptide-1 (GLP1) is a gut-derived incretin hormone with multiple actions in addition to control of glucose homeostasis (1) . Synthetic GLP1 receptor (GLP1R) agonists lower blood pressure in patients with type 2 diabetes
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experiments that the incretin effect, i.e., the augmented insulin secretion seen after oral vs i.v. glucose, is increased in insulin-resistant mice (3) and that the β-cell responsiveness to intravenous glucagon-like peptide-1 (GLP1) is augmented (3, 4
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). Incretin hormones are released after meal ingestion and account for up to 70% of postprandial insulin secretion ( 3 ). Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide are the most important incretin hormones. GLP-1 secretion is impaired
Danish Diabetes Academy, Odense University Hospital, Odense, Denmark
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Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark
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Department of Public Health, Research Unit of Epidemiology, Aarhus University, Aarhus, Denmark
Steno Diabetes Center Aarhus, Aarhus, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
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National Institute of Public Health, University of Southern Denmark, Odense, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
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for premature mortality ( 4 ). Glucagon-like peptide-1 (GLP-1) is a peptide hormone secreted from intestinal L-cells upon meal intake ( 5 ). GLP-1 stimulates insulin secretion in a glucose-dependent manner – as part of ‘the incretin effect’ – being
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
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Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
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Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Introduction Glucagon-like peptide 1 (GLP-1) is a gut-derived glucoregulatory hormone secreted in response to food consumption. Human GLP-1 is synthesised from the proglucagon gene and is secreted from the enteroendocrine L cells ( 1 ). Some
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Background Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have relevant antihyperglycemic effects and provide significant improvement on diabetes-related outcomes such as overweight and obesity, cardiovascular and renal impairment, and
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the treatment of glomerular diseases and key targets for the prevention and treatment of glomerular diseases ( 10 , 11 ). Glucagon-like peptide-1 (GLP-1) is an endogenous entero-insulinotropic hormone whose main target of action is GLP-1 receptor
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Department of Cardiology, Yanbian University Hospital, Yanji, China
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Introduction Glucagon-like peptide 1 (GLP-1) is one of the components of incretin, which can regulate the metabolism of the body and has a wide range of pharmacological effects ( 1 , 2 ). GLP-1R agonists like as liraglutide are currently