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-resistant mice is associated with increased islet GLP1 receptor (GLP1R) protein levels. We then examined the potential to improve islet function and glucose tolerance in glucose-intolerant insulin-resistant mice through GPR119 activation by administering a
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(GLP-1R). GLP-1R is expressed in islet β-cells and several extrapancreatic tissues, including the small inlet arteries, proximal tubules, and collecting ducts of the kidney ( 12 , 13 ). GLP-1R activity is significantly reduced in chronic kidney disease
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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
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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mechanism of action of incretin mimetic drugs is through the binding to glucagon-like peptide-1 receptor (GLP-1R) in pancreatic beta cells stimulating insulin secretion. The two most important natural incretin hormones are glucagon-like peptide-1 (GLP-1) and
Department of Endocrinology, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Population in Beijing, China) for GIPR SNP rs10423928 using second-stage HapMap data ( ftp://ftp.ncbi.nlm.nih.gov/hapmap/ ). Both GLP-1 and GIP are incretins. Previously, we demonstrated a correlation between GLP-1 receptor gene ( GLP-1R ) polymorphisms and
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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. Thus, only 10% of the native GLP-1 released from the enteroendocrine L cells reaches the systemic circulation ( 1 ). Activation of the GLP-1 receptor (GLP-1R) on the beta-cell enhances glucose-dependent secretion of insulin, thereby improving beta
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Department of Internal Medicine III, University Hospital Carl Gustav Carus Dresden, Dresden, Germany
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Comprehensive Heart Failure Center, Würzburg, Germany
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, 20 ). Long-acting GLP-1 receptor (GLP-1-R) agonists, e.g. semaglutide, are already in clinical use for the treatment of obesity. In adults with overweight or obesity and without diabetes mellitus, semaglutide leads to a mean weight loss of about 10
Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
Department of Ultrasound, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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group ( 35 ). Recent studies have shown that GLP-1R agonists exerted the reno-protective anti-inflammatory, anti-fibrosis, and anti-apoptosis effects, as well as reduction of renin-angiotensin-aldosterone system (RASS) ( 13 , 36 , 37 , 38 ). In the
Turku PET Centre, University of Turku, Turku, Finland
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Department of Radiology, University of Turku and Turku University Hospital, Turku, Finland
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) confirming the glucose dependency of GIP-secretion. However, the same relationship was not observed between increase in glucose and GLP-1 ( r P = 0.129, P = 0.722), even though GLP-1 (iAUC) but not GIP response was positively correlated with glucose