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ML Massa
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MI Borelli
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H Del Zotto
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JJ Gagliardino
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We correlated the changes in glucose-induced insulin secretion with those observed in glucose metabolism and hexokinase/glucokinase activity in islets from normal sucrose-fed hamsters. Blood glucose and insulin levels were measured in normal male hamsters fed with (S5) or without (C5) 10% sucrose in the drinking water for 5 weeks. Isolated islets (collagenase digestion) from both groups of animals were used to study insulin secretion, (14)CO(2) and (3)H(2)O production from D-[U-(14)C]-glucose and D-[5-(3)H]-glucose respectively, with 3.3 or 16.7 mM glucose in the medium, and hexokinase/glucokinase activity (fluorometric assay) in islet homogenates. Whereas S5 and C5 animals had comparable normal blood glucose levels, S5 showed higher insulin levels than C5 hamsters (2.3+/-0.1 vs 0.6+/-0.03 ng/ml, P<0.001). Islets from S5 hamsters released significantly more insulin than C5 islets in the presence of low and high glucose (3.3 mM glucose: 0.77+/-0.04 vs 0.20+/-0.06 pg/ng DNA/min, P<0.001; 16.7 mM glucose: 2.77+/-0.12 vs 0.85+/-0.06 pg/ng DNA/min, P<0.001) and produced significantly higher amounts of (14)CO(2) and (3)H(2)O at both glucose concentrations ((14)CO(2): 3.3 mM glucose: 0.27+/-0.01 vs 0.18+/-0.01, P<0.001; 16.7 mM glucose: 1.44+/-0.15 vs 0.96+/-0.08, P<0.02; (3)H(2)O: 3.3 mM glucose: 0.31+/-0.02 vs 0.15+/-0.01, P<0.001; 16.7 mM glucose: 1.46+/-0.20 vs 0.76+/-0.05 pmol glucose/ng DNA/min, P<0.005). The hexokinase K(m) and V(max) values from S5 animals were significantly higher than those from C5 ones (K(m): 100.14+/-7.01 vs 59.90+/- 3.95 microM, P<0.001; V(max): 0.010+/-0.0005 vs 0.008+/- 0.0006 pmol glucose/ng DNA/min, P<0.02). Conversely, the glucokinase K(m) value from S5 animals was significantly lower than in C5 animals (K(m): 15.31+/-2.64 vs 35.01+/-1.65 mM, P<0.001), whereas V(max) figures were within a comparable range in both groups (V(max): 0.048+/-0.009 vs 0.094+/-0.035 pmol glucose/ng DNA/min, not significant). The glucose phosphorylation ratio measured at 1 and 100 mM (hexokinase/glucokinase ratio) was significantly higher in S5 (0.26+/-0.02) than in C5 animals (0.11+/-0.01, P<0.005), and it was attributable to an increase in the hexokinase activity in S5 animals. In conclusion, sucrose administration increased the hexokinase/glucokinase activity ratio in the islets, which would condition the increase in glucose metabolism by beta-cells, and in beta-cell sensitivity and responsiveness to glucose. These results support the concept that increased hexokinase rather than glucokinase activity causes the beta-cell hypersensitivity to glucose, hexokinase being metabolically more active than glucokinase to up-regulate beta-cell function.

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James Cantley School of Medicine, University of Dundee, Dundee, Scotland, UK

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Decio Eizirik ULB Center for Diabetes Research, Medical Faculty, Université Libre De Bruxelles, Brussels, Belgium

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‘hyperinsulinise’ the peripheral tissues to reach physiological levels of the hormone in the portal system. Therefore, new disease-modifying therapies to protect and restore beta-cell function are urgently needed ( Martens et al. 2021 ). A final point to note at

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J Cantley School of Medicine, University of Dundee, Dundee, United Kingdom of Great Britain and Northern Ireland

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D L Eizirik ULB Center for Diabetes Research, Université Libre de Bruxelles Faculté de Médecine, Bruxelles, Belgium

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E Latres JDRF International, New York, NY, USA

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C M Dayan Cardiff University School of Medicine, Cardiff, United Kingdom of Great Britain and Northern Ireland

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the JDRF-DiabetesUK-INNODIA-nPOD Stockholm Symposium 2022
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the JDRF-DiabetesUK-INNODIA-nPOD Stockholm Symposium 2022

-insulitis observed in a T1DE2 donor. Further immune and beta cell characteristics of the endotypes are described in the boxes. Carmella Evans-Molina opened her lecture on ‘in vivo beta cell function in pre-clinical T1D diagnostics’ by discussing the

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Weiwei Xu Section of Endocrinology and Metabolism, Department of Medicine, Diabetes Discovery Research and Gender Medicine Laboratory, Tulane University Health Sciences Center, School of Medicine, and Southeast Louisiana Veterans Healthcare System Medical Center, New Orleans, Louisiana, USA

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Jamie Morford Section of Endocrinology and Metabolism, Department of Medicine, Diabetes Discovery Research and Gender Medicine Laboratory, Tulane University Health Sciences Center, School of Medicine, and Southeast Louisiana Veterans Healthcare System Medical Center, New Orleans, Louisiana, USA

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Franck Mauvais-Jarvis Section of Endocrinology and Metabolism, Department of Medicine, Diabetes Discovery Research and Gender Medicine Laboratory, Tulane University Health Sciences Center, School of Medicine, and Southeast Louisiana Veterans Healthcare System Medical Center, New Orleans, Louisiana, USA

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, Diabetes and Obesity 17 240 – 246 . ( https://doi.org/10.1097/MED.0b013e3283391fd1 ) 10.1097/MED.0b013e3283391fd1 Goodarzi MO Erickson S Port SC Jennrich RI Korenman SG 2005 beta-Cell function: a key pathological determinant in polycystic ovary

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Pieter-Jan Martens Clinical and Experimental Endocrinology (CEE), KU Leuven, Belgium

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Conny Gysemans Clinical and Experimental Endocrinology (CEE), KU Leuven, Belgium

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Chantal Mathieu Clinical and Experimental Endocrinology (CEE), KU Leuven, Belgium

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stresses the beta cells even further, this may result in a vicious circle, as was proven by the observation that the decline in beta cell function was less in intensively insulin-treated T1D patients ( The Diabetes Control and Complications Trial Research

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Frank H Bloomfield Liggins Institute, University of Auckland, Auckland, New Zealand

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glucose on the release of insulin in the sheep fetus . Journal of Endocrinology 85 121 – 129 . ( https://doi.org/10.1677/joe.0.0850121 ) 10.1677/joe.0.0850121 Fowden AL Barnes RJ Comline RS Silver M 1980 Pancreatic beta-cell function in

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Christine A Beamish Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA

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Yoon K Lee Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA

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A Osama Gaber Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA

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Priyanka Chanana Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA

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Edward A Graviss Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA
Department of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, Texas, USA

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Malgorzata Kloc Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA
Department of Cell and Microbiology, Weill Cornell Medical College, New York, New York, USA
Department of Genetics, The University of Texas Anderson Cancer Center, Houston, Texas, USA

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M Waleed Gaber Department of Pediatrics, Hematology-Oncology Section, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA
Department of Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas, USA

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Willa A Hsueh Department of Internal Medicine, The Ohio State University Diabetes and Metabolism Research Center, Columbus, Ohio, USA

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Omaima M Sabek Department of Surgery, Houston Methodist Research Institute, Houston, Texas, USA
Department of Cell and Microbiology, Weill Cornell Medical College, New York, New York, USA

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BA Pollock NK Casazza K Clemens TL Goree LL & Granger WM 2013 Associations of total and undercarboxylated osteocalcin with peripheral and hepatic insulin sensitivity and beta-cell function in overweight adults . Journal of Clinical

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Seokwon Jo Department of Integrative Biology & Physiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA

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Emilyn U Alejandro Department of Integrative Biology & Physiology, University of Minnesota Medical School, Minneapolis, Minnesota, USA

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composition of diet, length of diet fed prior to pregnancy to mimic obesity, and diet change post birth. Other animal studies in sheep and nonhuman primates also show maternal obesity is associated with altered beta-cell function or mass ( Ford et al. 2009

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Sarah J Richardson Islet Biology Group, Exeter Centre for Excellence in Diabetes (EXCEED), Institute of Biomedical and Clinical Sciences (IBCS), University of Exeter, RILD Level 4, Exeter, UK

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Alberto Pugliese Division of Diabetes Endocrinology and Metabolism, Departments of Medicine, Microbiology and Immunology, Diabetes Research Institute, Leonard Miller School of Medicine, University of Miami, Miami, Florida, USA

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support beta-cell function. The overall modest prevalence of insulitis at any given time suggests that the benefit of immunotherapy may be limited to those islets with insulitis and limit overall treatment efficacy. Combinatorial therapies should therefore

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Sandra K Szlapinski London, Ontario, Canada

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David J Hill Diabetes, Endocrinology and Metabolism, Lawson Health Research Institute, London, Ontario, Canada
Physiology and Pharmacology, Western University, London, Ontario, Canada

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loss of expression of insulin and key transcription factors for beta-cell function, such as PDX-1 and MAFA, and the MAFA-dependent glucose transporter 2 (GLUT2) ( Guo et al. 2013 ), or the appearance of a bihormonal cell phenotype with both insulin

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