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Sumaira Z Hasnain Immunity, Metabolic Diseases Program, Infection and Inflammation Program, Mater Research Institute, Translational Research Institute, University of Queensland, 37 Kent Street, Woolloongabba, Brisbane, Queensland 4102, Australia

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Johannes B Prins Immunity, Metabolic Diseases Program, Infection and Inflammation Program, Mater Research Institute, Translational Research Institute, University of Queensland, 37 Kent Street, Woolloongabba, Brisbane, Queensland 4102, Australia

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Michael A McGuckin Immunity, Metabolic Diseases Program, Infection and Inflammation Program, Mater Research Institute, Translational Research Institute, University of Queensland, 37 Kent Street, Woolloongabba, Brisbane, Queensland 4102, Australia

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production and closure of the KIR6.2 K + channel. This in turn leads to the depolarisation and influx of Ca 2 + , which drives the secretion of insulin granules. Insulin secretion is further boosted by incretin-receptor-mediated activation of protein kinase

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Vishal Musale Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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R Charlotte Moffett Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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Bosede Owolabi Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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J Michael Conlon Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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Peter R Flatt Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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Yasser H A Abdel-Wahab Diabetes Research Group, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland,

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of exenatide: the first antidiabetic agent to leverage the multiple benefits of the incretin hormone, GLP-1 . Expert Opinion on Drug Discovery 8 219 – 244 . ( https://doi.org/10.1517/17460441.2013.741580 ) Parthsarathy V Irwin N Hasib A

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Paola Moreno Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Bernardo Nuche-Berenguer Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Irene Gutiérrez-Rojas Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Alicia Acitores Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Verónica Sancho Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Isabel Valverde Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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Nieves González Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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María L Villanueva-Peñacarrillo Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain
Department of Metabolism, CIBERDEM, Nutrition and Hormones, IIS-Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain

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-1 (GLP-1 or GCG as listed in the HUGO database), an incretin hormone with anti-diabetic properties, exerts insulin-like effects upon glucose transport (GT) and metabolism in the liver, skeletal muscle, and fat of humans and rats ( Valverde et al

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Ying Ying School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China

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Huazhang Zhu School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China

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Zhen Liang School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China
School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China

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Xiaosong Ma School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China

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Shiwei Li School of Medicine, Department of Geriatric, Shenzhen University Diabetes Center, Shenzhen University, Shenzhen 518060, China

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of palmitate-induced cardiomyocyte apoptosis has not been determined thus far. Glucagon-like peptide 1 (GLP1) is an incretin hormone synthesized and secreted by intestinal L-cells and stimulates insulin secretion from pancreatic b-cells in a glucose

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Jin-Seung Choung College of Pharmacy and Gachon Institute of Pharmaceutical Science, Gachon University, Incheon, Republic of Korea
Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea

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Young-Sun Lee Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea

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Hee-Sook Jun College of Pharmacy and Gachon Institute of Pharmaceutical Science, Gachon University, Incheon, Republic of Korea
Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea
Gachon Medical Research Institute, Gil Hospital, Incheon, Republic of Korea

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Introduction Glucagon-like peptide-1 (GLP1) is an incretin hormone that is secreted from enteroendocrine gastrointestinal L cells after meal ( Layer et al . 1995 ). GLP1 controls glucose homeostasis in many organs; it has a glucose

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Rune Ehrenreich Kuhre Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, the Panum Institute, University of Copenhagen, Copenhagen, Denmark

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Nicolai Jacob Wewer Albrechtsen Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, the Panum Institute, University of Copenhagen, Copenhagen, Denmark

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Carolyn Fiona Deacon Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, the Panum Institute, University of Copenhagen, Copenhagen, Denmark

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Emilie Balk-Møller Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, the Panum Institute, University of Copenhagen, Copenhagen, Denmark

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Jens Frederik Rehfeld Department of Clinical Biochemistry Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Frank Reimann Cambridge Institute for Medical Research and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, United Kingdom

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Fiona Mary Gribble Cambridge Institute for Medical Research and MRC Metabolic Diseases Unit, University of Cambridge, Cambridge, United Kingdom

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Jens Juul Holst Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, the Panum Institute, University of Copenhagen, Copenhagen, Denmark

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, and is particularly known for its incretin actions , that is, the enhancement of meal-stimulated insulin secretion. This serves to limit postprandial blood glucose levels ( Holst 2007 ), and therefore, GLP-1-based drugs are used to treat type II

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Horng-Yih Ou
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Hung-Tsung Wu Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan
Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Feng-Hwa Lu Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Yu-Chu Su Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Hao-Chang Hung
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Jin-Shang Wu Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Yi-Ching Yang Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Chao-Liang Wu Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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Chih-Jen Chang Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan
Division of Endocrinology and Metabolism, Research Center of Herbal Medicine, Department of Family Medicine, College of Medicine, Department of Internal Medicine, National Cheng Kung University Hospital, 138, Sheng‐Li Road, Tainan 70403, Taiwan

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agonist AS2575959 exhibits glucose metabolism improvement and synergistic effect with sitagliptin on insulin and incretin secretion . Life Sciences 94 115 – 121 . ( doi:10.1016/j.lfs.2013.11.010 ). Wang SR Pessah M Infante J Catala D Salvat

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Stacey N Walters Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia

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Jude Luzuriaga Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia

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Jeng Yie Chan Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia

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Shane T Grey Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia
Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia

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D Ross Laybutt Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia
Garvan Institute of Medical Research, St Vincent's Clinical School, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia

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receptor, G-protein-coupled receptor 40 ( Gpr40 ( Ffar1 )), and the incretin GLP-1 receptor ( Glp1r ) ( Fig. 3C ). Expression of all the tested β-cell differentiation genes was at least partially restored in islet grafts from diabetic-normalized mice ( Fig

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Thierry Brun Department of Cell Physiology and Metabolism, University Medical Centre, 1211 Geneva 4, Switzerland

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Benoit R Gauthier Department of Cell Physiology and Metabolism, University Medical Centre, 1211 Geneva 4, Switzerland

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). Furthermore, endogenous Pax4 mRNA levels were also induced in human islets by glucose, activin A and betacellulin. In addition, the incretin glucagon-like peptide (GLP)-1, a new therapeutic agent for the treatment of diabetes, which has been shown to increase

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Matthias Laudes Department of Internal Medicine II, University of Cologne, Kerpener Strasse 62, 50924 Cologne, Germany

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( Smith 2007 ). However, studies on a potential mechanism whereby TCF7L2 might influence diabetes risk revealed that pathogenetic SNPs are related to impaired insulin secretion and disturbed effects of the incretin system, which suggests that WNT

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