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Meeting Abstracts

314-OR: Synaptotagmin-9 Regulates Early Phase Insulin Secretion by Regulating Tomosyn-1

MD MOSTAFIZUR RAHMAN, HAIFA ALSHARIF, SUSHANT BHATNAGAR

Diabetes 2022;71(Supplement_1):314-OR

DOI: https://doi.org/10.2337/db22-314-OR

Published: 01 June 2022

View article titled, 314-OR: Synaptotagmin-9 Regulates Early Phase Insulin Secretion by Regulating Tomosyn-1

Journal Articles

Cerebrovascular Safety of Sulfonylureas: The Role of K_ATP Channels in Neuroprotection and the Risk of Stroke in Patients With Type 2 Diabetes

Rui Liu, Haitao Wang, Baofeng Xu, Wenliang Chen, Ekaterina Turlova, Nan Dong, Christopher L.F. Sun, Yangqingqin Lu, Hanhui Fu, Ranran Shi, Andrew Barszczyk, Dongzi Yang, Tianru Jin, Edoardo Mannucci, Zhong-Ping Feng, Hong-Shuo Sun

Diabetes 2016;65(9):2795–2809

DOI: https://doi.org/10.2337/db15-1737

Published: 13 May 2016

View article titled, Cerebrovascular Safety of Sulfonylureas: The Role of KATP Channels in Neuroprotection and the Risk of Stroke in Patients With Type 2 Diabetes

Journal Articles

Human Insulinomas Show Distinct Patterns of Insulin Secretion In Vitro

Jean-Claude Henquin, Myriam Nenquin, Yves Guiot, Jacques Rahier, Christine Sempoux

Diabetes 2015;64(10):3543–3553

DOI: https://doi.org/10.2337/db15-0527

Published: 26 June 2015

View article titled, Human Insulinomas Show Distinct Patterns of Insulin Secretion In Vitro

Includes: Supplementary data

Journal Articles

Congenital Hyperinsulinism Caused by Hexokinase I Expression or Glucokinase-Activating Mutation in a Subset of β-Cells

Jean-Claude Henquin, Christine Sempoux, Joelle Marchandise, Sebastien Godecharles, Yves Guiot, Myriam Nenquin, Jacques Rahier

Diabetes 2013;62(5):1689–1696

DOI: https://doi.org/10.2337/db12-1414

Published: 16 April 2013

View article titled, Congenital Hyperinsulinism Caused by Hexokinase I Expression or Glucokinase-Activating Mutation in a Subset of β-Cells

Includes: Supplementary data

Journal Articles

Stimulatory Effect of Insulin on Glucose Uptake by Muscle Involves the Central Nervous System in Insulin-Sensitive Mice

Claudia P. Coomans, Nienke R. Biermasz, Janine J. Geerling, Bruno Guigas, Patrick C.N. Rensen, Louis M. Havekes, Johannes A. Romijn

Diabetes 2011;60(12):3132–3140

DOI: https://doi.org/10.2337/db10-1100

Published: 13 November 2011

View article titled, Stimulatory Effect of Insulin on Glucose Uptake by Muscle Involves the Central Nervous System in Insulin-Sensitive Mice

Includes: Supplementary data

Journal Articles

ATP-Sensitive K⁺ Channel Mediates the Zinc Switch-Off Signal for Glucagon Response During Glucose Deprivation

Michela Slucca, Jamie S. Harmon, Elizabeth A. Oseid, Joseph Bryan, R. Paul Robertson

Diabetes 2010;59(1):128–134

DOI: https://doi.org/10.2337/db09-1098

Published: 06 October 2009

View article titled, ATP-Sensitive K+ Channel Mediates the Zinc Switch-Off Signal for Glucagon Response During Glucose Deprivation

Journal Articles

Studies of Association of Variants Near the HHEX, CDKN2A/B, and IGF2BP2 Genes With Type 2 Diabetes and Impaired Insulin Release in 10,705 Danish Subjects: Validation and Extension of Genome-Wide Association Studies

Niels Grarup, Chrisian S. Rose, Ehm A. Andersson, Gitte Andersen, Arne L. Nielsen, Anders Albrechtsen, Jesper O. Clausen, Signe S. Rasmussen, Torben Jørgensen, Annelli Sandbæk, Torsten Lauritzen, Ole Schmitz, Torben Hansen, Oluf Pedersen

Diabetes 2007;56(12):3105–3111

DOI: https://doi.org/10.2337/db07-0856

Published: 01 December 2007

View article titled, Studies of Association of Variants Near the HHEX, CDKN2A/B, and IGF2BP2 Genes With Type 2 Diabetes and Impaired Insulin Release in 10,705 Danish Subjects: Validation and Extension of Genome-Wide Association Studies

Includes: Supplementary data

Journal Articles

Congenital Hyperinsulinism–Associated ABCC8 Mutations That Cause Defective Trafficking of ATP-Sensitive K⁺ Channels: Identification and Rescue

Fei-Fei Yan, Yu-Wen Lin, Courtney MacMullen, Arupa Ganguly, Charles A. Stanley, Show-Ling Shyng

Diabetes 2007;56(9):2339–2348

DOI: https://doi.org/10.2337/db07-0150

Published: 01 September 2007

View article titled, Congenital Hyperinsulinism–Associated ABCC8 Mutations That Cause Defective Trafficking of ATP-Sensitive K+ Channels: Identification and Rescue

Includes: Supplementary data

Journal Articles

The Actions of a Novel Potent Islet β-Cell–Specific ATP-Sensitive K⁺ Channel Opener Can Be Modulated by Syntaxin-1A Acting on Sulfonylurea Receptor 1

Betty Ng, Youhou Kang, Chadwick L. Elias, Yan He, Huanli Xie, John B. Hansen, Philip Wahl, Herbert Y. Gaisano

Diabetes 2007;56(8):2124–2134

DOI: https://doi.org/10.2337/db07-0030

Published: 01 August 2007

View article titled, The Actions of a Novel Potent Islet β-Cell–Specific ATP-Sensitive K+ Channel Opener Can Be Modulated by Syntaxin-1A Acting on Sulfonylurea Receptor 1

Includes: Supplementary data

Journal Articles

Cx36-Mediated Coupling Reduces β-Cell Heterogeneity, Confines the Stimulating Glucose Concentration Range, and Affects Insulin Release Kinetics

Stephan Speier, Asllan Gjinovci, Anne Charollais, Paolo Meda, Marjan Rupnik

Diabetes 2007;56(4):1078–1086

DOI: https://doi.org/10.2337/db06-0232

Published: 01 April 2007

View article titled, Cx36-Mediated Coupling Reduces β-Cell Heterogeneity, Confines the Stimulating Glucose Concentration Range, and Affects Insulin Release Kinetics

Journal Articles

Sulfonylurea Compounds Uncouple the Glucose Dependence of the Insulinotropic Effect of Glucagon-Like Peptide 1

Jocelyn de Heer, Jens J. Holst

Diabetes 2007;56(2):438–443

DOI: https://doi.org/10.2337/db06-0738

Published: 01 February 2007

View article titled, Sulfonylurea Compounds Uncouple the Glucose Dependence of the Insulinotropic Effect of Glucagon-Like Peptide 1

Journal Articles

An ATP-Binding Mutation (G334D) in KCNJ11 Is Associated With a Sulfonylurea-Insensitive Form of Developmental Delay, Epilepsy, and Neonatal Diabetes

Ricard Masia, Joseph C. Koster, Stefano Tumini, Francesco Chiarelli, Carlo Colombo, Colin G. Nichols, Fabrizio Barbetti

Diabetes 2007;56(2):328–336

DOI: https://doi.org/10.2337/db06-1275

Published: 01 February 2007

View article titled, An ATP-Binding Mutation (G334D) in KCNJ11 Is Associated With a Sulfonylurea-Insensitive Form of Developmental Delay, Epilepsy, and Neonatal Diabetes

Journal Articles

A Kir6.2 Mutation Causing Neonatal Diabetes Impairs Electrical Activity and Insulin Secretion From INS-1 β-Cells

Andrei I. Tarasov, Hannah J. Welters, Sabine Senkel, Gerhart U. Ryffel, Andrew T. Hattersley, Noel G. Morgan, Frances M. Ashcroft

Diabetes 2006;55(11):3075–3082

DOI: https://doi.org/10.2337/db06-0637

Published: 01 November 2006

View article titled, A Kir6.2 Mutation Causing Neonatal Diabetes Impairs Electrical Activity and Insulin Secretion From INS-1 β-Cells

Journal Articles

Mutations at the Same Residue (R50) of Kir6.2 (KCNJ11) That Cause Neonatal Diabetes Produce Different Functional Effects

Kenju Shimomura, Christophe A.J. Girard, Peter Proks, Joanna Nazim, Jonathan D. Lippiat, Franco Cerutti, Renata Lorini, Sian Ellard, Andrew T. Hattersley, Fabrizio Barbetti, Frances M. Ashcroft

Diabetes 2006;55(6):1705–1712

DOI: https://doi.org/10.2337/db05-1640

Published: 01 June 2006

View article titled, Mutations at the Same Residue (R50) of Kir6.2 (KCNJ11) That Cause Neonatal Diabetes Produce Different Functional Effects

Journal Articles

ATP and Sulfonylurea Sensitivity of Mutant ATP-Sensitive K⁺ Channels in Neonatal Diabetes: Implications for Pharmacogenomic Therapy

Joseph C. Koster, Maria S. Remedi, Crystal Dao, Colin G. Nichols

Diabetes 2005;54(9):2645–2654

DOI: https://doi.org/10.2337/diabetes.54.9.2645

Published: 01 September 2005

View article titled, ATP and Sulfonylurea Sensitivity of Mutant ATP-Sensitive K+ Channels in Neonatal Diabetes: Implications for Pharmacogenomic Therapy

Journal Articles

Desensitization of Insulin Secretion by Depolarizing Insulin Secretagogues

Ingo Rustenbeck, Antje Wienbergen, Claudia Bleck, Anne Jörns

Diabetes 2004;53(suppl_3):S140–S150

DOI: https://doi.org/10.2337/diabetes.53.suppl_3.S140

Published: 01 December 2004

View article titled, Desensitization of Insulin Secretion by Depolarizing Insulin Secretagogues

Journal Articles

Hypothalamic ATP-sensitive K ⁺ Channels Play a Key Role in Sensing Hypoglycemia and Triggering Counterregulatory Epinephrine and Glucagon Responses

Mark L. Evans, Rory J. McCrimmon, Daniel E. Flanagan, Tara Keshavarz, Xiaoning Fan, Ewan C. McNay, Ralph J. Jacob, Robert S. Sherwin

Diabetes 2004;53(10):2542–2551

DOI: https://doi.org/10.2337/diabetes.53.10.2542

Published: 01 October 2004

View article titled, Hypothalamic ATP-sensitive K + Channels Play a Key Role in Sensing Hypoglycemia and Triggering Counterregulatory Epinephrine and Glucagon Responses

Journal Articles

Glucose- and Interleukin-1β-Induced β-Cell Apoptosis Requires Ca²⁺ Influx and Extracellular Signal-Regulated Kinase (ERK) 1/2 Activation and Is Prevented by a Sulfonylurea Receptor 1/Inwardly Rectifying K⁺ Channel 6.2 (SUR/Kir6.2) Selective Potassium Channel Opener in Human Islets

Kathrin Maedler, Joachim Størling, Jeppe Sturis, Richard A. Zuellig, Giatgen A. Spinas, Per O.G. Arkhammar, Thomas Mandrup-Poulsen, Marc Y. Donath

Diabetes 2004;53(7):1706–1713

DOI: https://doi.org/10.2337/diabetes.53.7.1706

Published: 01 July 2004

View article titled, Glucose- and Interleukin-1β-Induced β-Cell Apoptosis Requires Ca2+ Influx and Extracellular Signal-Regulated Kinase (ERK) 1/2 Activation and Is Prevented by a Sulfonylurea Receptor 1/Inwardly Rectifying K+ Channel 6.2 (SUR/Kir6.2) Selective Potassium Channel Opener in Human Islets

Journal Articles

Sulfonylureas Rapidly Cross Phospholipid Bilayer Membranes by a Free-Diffusion Mechanism

Frits Kamp, Nadeem Kizilbash, Barbara E. Corkey, Per-Olof Berggren, James A. Hamilton

Diabetes 2003;52(10):2526–2531

DOI: https://doi.org/10.2337/diabetes.52.10.2526

Published: 01 October 2003

View article titled, Sulfonylureas Rapidly Cross Phospholipid Bilayer Membranes by a Free-Diffusion Mechanism

Journal Articles

Clinical and Molecular Characterization of a Dominant Form of Congenital Hyperinsulinism Caused by a Mutation in the High-Affinity Sulfonylurea Receptor

Paul S. Thornton, Courtney MacMullen, Arupa Ganguly, Eduardo Ruchelli, Linda Steinkrauss, Ana Crane, Lydia Aguilar-Bryan, Charles A. Stanley

Diabetes 2003;52(9):2403–2410

DOI: https://doi.org/10.2337/diabetes.52.9.2403

Published: 01 September 2003

View article titled, Clinical and Molecular Characterization of a Dominant Form of Congenital Hyperinsulinism Caused by a Mutation in the High-Affinity Sulfonylurea Receptor

NARROW

314-OR: Synaptotagmin-9 Regulates Early Phase Insulin Secretion by Regulating Tomosyn-1

Cerebrovascular Safety of Sulfonylureas: The Role of K_ATP Channels in Neuroprotection and the Risk of Stroke in Patients With Type 2 Diabetes

Human Insulinomas Show Distinct Patterns of Insulin Secretion In Vitro

Congenital Hyperinsulinism Caused by Hexokinase I Expression or Glucokinase-Activating Mutation in a Subset of β-Cells

Stimulatory Effect of Insulin on Glucose Uptake by Muscle Involves the Central Nervous System in Insulin-Sensitive Mice

ATP-Sensitive K⁺ Channel Mediates the Zinc Switch-Off Signal for Glucagon Response During Glucose Deprivation

Studies of Association of Variants Near the HHEX, CDKN2A/B, and IGF2BP2 Genes With Type 2 Diabetes and Impaired Insulin Release in 10,705 Danish Subjects: Validation and Extension of Genome-Wide Association Studies

Congenital Hyperinsulinism–Associated ABCC8 Mutations That Cause Defective Trafficking of ATP-Sensitive K⁺ Channels: Identification and Rescue

The Actions of a Novel Potent Islet β-Cell–Specific ATP-Sensitive K⁺ Channel Opener Can Be Modulated by Syntaxin-1A Acting on Sulfonylurea Receptor 1

Cx36-Mediated Coupling Reduces β-Cell Heterogeneity, Confines the Stimulating Glucose Concentration Range, and Affects Insulin Release Kinetics

Sulfonylurea Compounds Uncouple the Glucose Dependence of the Insulinotropic Effect of Glucagon-Like Peptide 1

An ATP-Binding Mutation (G334D) in KCNJ11 Is Associated With a Sulfonylurea-Insensitive Form of Developmental Delay, Epilepsy, and Neonatal Diabetes

A Kir6.2 Mutation Causing Neonatal Diabetes Impairs Electrical Activity and Insulin Secretion From INS-1 β-Cells

Mutations at the Same Residue (R50) of Kir6.2 (KCNJ11) That Cause Neonatal Diabetes Produce Different Functional Effects

ATP and Sulfonylurea Sensitivity of Mutant ATP-Sensitive K⁺ Channels in Neonatal Diabetes: Implications for Pharmacogenomic Therapy

Desensitization of Insulin Secretion by Depolarizing Insulin Secretagogues

Hypothalamic ATP-sensitive K ⁺ Channels Play a Key Role in Sensing Hypoglycemia and Triggering Counterregulatory Epinephrine and Glucagon Responses

Glucose- and Interleukin-1β-Induced β-Cell Apoptosis Requires Ca²⁺ Influx and Extracellular Signal-Regulated Kinase (ERK) 1/2 Activation and Is Prevented by a Sulfonylurea Receptor 1/Inwardly Rectifying K⁺ Channel 6.2 (SUR/Kir6.2) Selective Potassium Channel Opener in Human Islets

Sulfonylureas Rapidly Cross Phospholipid Bilayer Membranes by a Free-Diffusion Mechanism

Clinical and Molecular Characterization of a Dominant Form of Congenital Hyperinsulinism Caused by a Mutation in the High-Affinity Sulfonylurea Receptor

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