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Lawson Health Research Institute, Medicine, Microbiology and Immunology, Paediatrics, St Joseph's Health Care, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2 Departments of
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Lawson Health Research Institute, Medicine, Microbiology and Immunology, Paediatrics, St Joseph's Health Care, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2 Departments of
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Lawson Health Research Institute, Medicine, Microbiology and Immunology, Paediatrics, St Joseph's Health Care, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2 Departments of
Lawson Health Research Institute, Medicine, Microbiology and Immunology, Paediatrics, St Joseph's Health Care, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2 Departments of
Lawson Health Research Institute, Medicine, Microbiology and Immunology, Paediatrics, St Joseph's Health Care, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2 Departments of
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Introduction Type 1 diabetes originates with the autoimmune-mediated destruction of pancreatic β-cells, and is characterized by a change in cytokine secretion from a helper T-cell (Th) 2 phenotype with relatively low levels of interferon γ (IFNγ
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Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
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2 diabetes mellitus (T2D) ( Turnbaugh et al . 2006 , Qin et al . 2012 , Ridaura et al . 2013 , Lynch & Pedersen 2016 ). Ablating gut microbiota, as in germ free (GF) mice, improves glucose tolerance and renders mice resistant to diet
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approved in many countries for use in patients with type 2 diabetes. A number of others are in late-stage clinical development. All these drugs act to enhance incretin signalling not only in pancreatic β-cells, but also in other pancreatic cells and tissues
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pancreatic islets are known to retain epigenetic marks of active insulin promoter ( Mutskov et al . 2007 ), such islet-derived cells are believed to be of potential importance for cell replacement therapy in diabetes. Though mouse insulin-producing cells are
Bayer HealthCare, Biotechnology, 800 Dwight Way, Berkeley, California 94701, USA
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Bayer HealthCare, Biotechnology, 800 Dwight Way, Berkeley, California 94701, USA
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Bayer HealthCare, Biotechnology, 800 Dwight Way, Berkeley, California 94701, USA
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development for the treatment of type 2 diabetes ( Weber 2004 and for review, see Knudsen 2004 ). One frequently observed side-effect of GLP-1, or its analogues, is nausea and vomiting correlating with the inhibition of gastrointestinal (GI) motility ( Buse
School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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weight loss ( Turton et al. 1996 , Larsen et al. 2001 ). Consequently, GLP-1 has been put forward as a potential drug candidate for type 2 diabetes mellitus, and GLP-1 analogues are currently undergoing clinical trials ( Holz & Chepurny 2003
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Department of Ophthalmology and Visual Sciences, University of Alberta, Edmonton, Alberta, Canada
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Department of Physiology, University of Alberta, Edmonton, Alberta, Canada
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Introduction Type 2 diabetes (T2D) is a metabolic disorder associated with chronic hyperglycemia and disruptions in carbohydrate, lipid, and protein metabolism, resulting from decreased production or altered responsiveness to insulin ( Reaven
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Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK
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Introduction There has been an alarming increase, of epidemic proportions, in both obesity and diabetes in the general population with increased cardiovascular risk associated with type 2 diabetes mellitus (T2DM) and/or metabolic syndrome (MetS
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Introduction Both type 1 and type 2 diabetes have been associated with pancreatic β-cell dysfunction, with reduced glucose-stimulated insulin secretion and decreased β-cell mass due to impaired β-cell proliferation and survival ( Butler et al
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. 2005 ). Furthermore, variations within IP3R3 have been identified as a risk factor for type 1 diabetes in humans ( Roach et al . 2006 ). IP3R1 is the most abundant isoform in mouse brain and pancreatic β-cells ( De Smedt et al . 1997 , Lee & Laychock