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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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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
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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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
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Department of Medicine (AH), Walter and Eliza Hall Institute of Medical Research, Harry Perkins Institute of Medical Research, The School of Medical Sciences Edith Cowan University, Austin Hospital, University of Melbourne, Level 7, Lance Townsend Building, Studley Road, Heidelberg, Victoria 3084, Australia
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when there is failure of the β-cell to secrete adequate amounts of insulin ( Kahn 2003 , Andrikopoulos 2010 ). Glucose is the predominant nutrient for insulin secretion, which enters the β-cell via the glucose transporter GLUT-2 and gets phosphorylated
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. 2004 ), promoting β-cell survival, and from glucose ( Rondas et al . 2011 , 2012 , Arous et al . 2013 ), stimulating insulin secretion both in vitro and in vivo ( Cai et al . 2012 ). Absence of Shb has no effect on β-cell proliferation, but
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all five receptors are expressed in the islets ( Ludvigsen et al . 2004 ). Results from studies using SSTR-deficient mice (SSTR1, SSTR2 or SSTR5) revealed changes in both basal and stimulated insulin secretion ( Strowski et al . 2000 , Wang et al
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multiple genes encoding proteins involved in insulin signaling, insulin secretion and intermediary metabolism ( Stern 2000 , Kahn et al . 2006 ). Regardless, the detrimental impact of diet-induced MO on the long-term health, adiposity and metabolism of
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experimental procedure. Insulin secretion stimulation To adapt isolated islets to a baseline glucose concentration (5.6 mmol/l), they were preincubated for 60 min in 1 ml of normal Krebs–Ringer solution ((mmol/l): NaCl, 115; NaHCO 3 , 24; KCl, 1.6; MgCl6H 2 O
Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
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, producing hyperinsulinemia during fasting and feeding states ( Shafrir 1996 ). Why is glucose-induced insulin secretion upregulated in obese human beings and experimental animal models? Several hypotheses have been proposed. One hypothesis is largely
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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