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stream, they have an important clinical impact. Diminished glucose-stimulated insulin secretion (GSIS) and β-cell failure correlate with DM development ( Jensen et al . 2008 , Newsholme & Krause 2012 ), and consequently it is important to determine the
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
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Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
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Division of Cellular and Molecular Medicine, Departments of Metabolic Medicine, Endocrinology and Diabetes, Department of Medical Physiology, Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan
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Introduction Insulin secreted from pancreatic β-cells plays a pivotal role in the maintenance of glucose homeostasis. Insulin secretion is regulated by various factors including nutrients such as glucose, amino acids, and fatty acids
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). This peptide belongs to the insulin, gastric intestinal peptide, and endocrine peptide family. Several studies have shown that preptin can enhance insulin secretion, while infusion of isolated pancreases with preptin antibodies significantly reduces
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the context of diabetes mellitus, n-3 PUFAs have anti-inflammatory and insulin-sensitizing functions ( Kalupahana et al . 2011 ). However, the effect of n-3 PUFAs on insulin secretion from pancreatic β-cells is not well recognized. Defects in insulin
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lead to an impairment of insulin secretion. Thus insulin-secretion defects have been observed in mice and beta cells from mice with a beta-cell-specific insulin receptor ( Kido et al. 2000 ) or IRS-1 ( Kulkarni et al. 1999 a , Kido et al. 2000
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Introduction Hormonal disturbance, in either secretion amount or function, often occurs in parallel with impairment of glucose/lipid/protein metabolism in obesity. Two pivotal hormones, insulin and growth hormone (GH), which synergistically
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Université Côte d’Azur, CNRS, LP2M, Nice, France
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Université Côte d’Azur, CHU, Inserm, CNRS, IRCAN, Nice, France
Université Côte d’Azur, CHU, CNRS, LP2M, Nice, France
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linked to insulin secretion has several exclusive features. First, glucose transport is not limiting for its metabolism, and it results in a rapid equilibrium between intracellular and extracellular glucose at all glycemic levels. The second particular
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Department of Biological Sciences, Laboratory of Biosystems, Federal University of São Paulo, Diadema, São Paulo, Brazil
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stimulatory effect of melatonin in the pancreas ( Peschke & Peschke 1998 ), there are consistent scientific evidences supporting that melatonin inhibits insulin secretion in islets ( Peschke et al. 2000 ) and clonal beta cell lines ( Mühlbauer & Peschke 2007
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
UMR859, INSERM UMR859, INSERM UMR837, CHU Lille, Faculty of Medicine, Université Lille Nord de France, 1 Place de Verdun, F-59000 Lille, France
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specific deletion of TSC2 in β-cells induced β-cell apoptosis and reduced insulin secretion, after a first phase of β-cell mass expansion ( Shigeyama et al . 2008 ). In the rat, l -leucine, an amino acid known to induce mTORC1 activation, negatively
Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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Department of Pharmacology, Hanoi Medical University, Hanoi, Vietnam
Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden
Institute of Material Medica, Hanoi, Vietnam
Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
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-cell K-ATP channel (DeFronzo1999, Brown et al. 2004 ). Glucose-stimulated biphasic insulin secretion involves at least two signaling pathways, the K-ATP channel-dependent and K-ATP channel-independent pathways respectively ( Chow et al. 1995