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Journal Articles

Phenotypic Characterization of Congenital Hyperinsulinism Due to Novel Activating Glucokinase Mutations

Changhong Li, Christine A. Juliana, Yue Yuan, Ming Li, Ming Lu, Pan Chen, Kara E. Boodhansingh, Nicolai M. Doliba, Tricia R. Bhatti, N. Scott Adzick, Charles A. Stanley, Diva D. De León

Diabetes 2023;72(12):1809–1819

https://doi.org/10.2337/db23-0465

Published: 19 September 2023

View article titled, Phenotypic Characterization of Congenital Hyperinsulinism Due to Novel Activating Glucokinase Mutations

Meeting Abstracts

Functional Maturation of Pancreatic ß Cells during Development

DIANA E. STANESCU, CHANGHONG LI, JUXIANG YANG, DAPHNE YAU, CHARLES A. STANLEY

Diabetes 2018;67(Supplement_1):2131-P

https://doi.org/10.2337/db18-2131-P

Published: 01 July 2018

View article titled, Functional Maturation of Pancreatic ß Cells during Development

Journal Articles

Regulation of K_ATP Channel Trafficking in Pancreatic β-Cells by Protein Histidine Phosphorylation

Shekhar Srivastava, Zhai Li, Irfana Soomro, Ying Sun, Jianhui Wang, Li Bao, William A. Coetzee, Charles A. Stanley, Chonghong Li, Edward Y. Skolnik

Diabetes 2018;67(5):849–860

https://doi.org/10.2337/db17-1433

Published: 12 February 2018

View article titled, Regulation of KATP Channel Trafficking in Pancreatic β-Cells by Protein Histidine Phosphorylation

Includes: Supplementary data

Journal Articles

Functional and Metabolomic Consequences of K_ATP Channel Inactivation in Human Islets

Changhong Li, Amanda M. Ackermann, Kara E. Boodhansingh, Tricia R. Bhatti, Chengyang Liu, Jonathan Schug, Nicolai Doliba, Bing Han, Karen E. Cosgrove, Indraneel Banerjee, Franz M. Matschinsky, Itzhak Nissim, Klaus H. Kaestner, Ali Naji, N. Scott Adzick, Mark J. Dunne, Charles A. Stanley, Diva D. De León

Diabetes 2017;66(7):1901–1913

https://doi.org/10.2337/db17-0029

Published: 25 April 2017

View article titled, Functional and Metabolomic Consequences of KATP Channel Inactivation in Human Islets

Includes: Supplementary data

Journal Articles

GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Fasting Blood Glucose Levels in Congenital Hyperinsulinism Owing to Inactivating Mutations in the ATP-Sensitive K⁺ Channel

Andrew C. Calabria, Changhong Li, Paul R. Gallagher, Charles A. Stanley, Diva D. De León

Diabetes 2012;61(10):2585–2591

https://doi.org/10.2337/db12-0166

Published: 13 September 2012

View article titled, GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Fasting Blood Glucose Levels in Congenital Hyperinsulinism Owing to Inactivating Mutations in the ATP-Sensitive K+ Channel

Journal Articles

Diazoxide-Unresponsive Congenital Hyperinsulinism in Children With Dominant Mutations of the β-Cell Sulfonylurea Receptor SUR1

Courtney M. MacMullen, Qing Zhou, Kara E. Snider, Paul H. Tewson, Susan A. Becker, Ali Rahim Aziz, Arupa Ganguly, Show-Ling Shyng, Charles A. Stanley

Diabetes 2011;60(6):1797–1804

https://doi.org/10.2337/db10-1631

Published: 21 May 2011

View article titled, Diazoxide-Unresponsive Congenital Hyperinsulinism in Children With Dominant Mutations of the β-Cell Sulfonylurea Receptor SUR1

Journal Articles

Extremes of Clinical and Enzymatic Phenotypes in Children With Hyperinsulinism Caused by Glucokinase Activating Mutations

Samir Sayed, David R. Langdon, Stella Odili, Pan Chen, Carol Buettger, Alisa B. Schiffman, Mariko Suchi, Rebecca Taub, Joseph Grimsby, Franz M. Matschinsky, Charles A. Stanley

Diabetes 2009;58(6):1419–1427

https://doi.org/10.2337/db08-1792

Published: 31 March 2009

View article titled, Extremes of Clinical and Enzymatic Phenotypes in Children With Hyperinsulinism Caused by Glucokinase Activating Mutations

Journal Articles

Follow-Up Analysis of Genome-Wide Association Data Identifies Novel Loci for Type 1 Diabetes

Diabetes 2009;58(1):290–295

https://doi.org/10.2337/db08-1022

Published: 01 January 2009

View article titled, Follow-Up Analysis of Genome-Wide Association Data Identifies Novel Loci for Type 1 Diabetes

Includes: Supplementary data

Journal Articles

A Novel Susceptibility Locus for Type 1 Diabetes on Chr12q13 Identified by a Genome-Wide Association Study

Diabetes 2008;57(4):1143–1146

https://doi.org/10.2337/db07-1305

Published: 01 April 2008

View article titled, A Novel Susceptibility Locus for Type 1 Diabetes on Chr12q13 Identified by a Genome-Wide Association Study

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

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: <subtitle>Identification and Rescue</subtitle>

Includes: Supplementary data

Journal Articles

A Mutation in the TMD0-L0 Region of Sulfonylurea Receptor-1 (L225P) Causes Permanent Neonatal Diabetes Mellitus (PNDM)

Ricard Masia, Diva D. De Leon, Courtney MacMullen, Heather McKnight, Charles A. Stanley, Colin G. Nichols

Diabetes 2007;56(5):1357–1362

https://doi.org/10.2337/db06-1746

Published: 01 May 2007

View article titled, A Mutation in the TMD0-L0 Region of Sulfonylurea Receptor-1 (L225P) Causes Permanent Neonatal Diabetes Mellitus (PNDM)

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

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

Journal Articles

Glutaminolysis and Insulin Secretion: From Bedside to Bench and Back

Andrea Kelly, Changhong Li, Zhiyong Gao, Charles A. Stanley, Franz M. Matschinsky

Diabetes 2002;51(suppl_3):S421–S426

https://doi.org/10.2337/diabetes.51.2007.S421

Published: 01 December 2002

View article titled, Glutaminolysis and Insulin Secretion: <subtitle>From Bedside to Bench and Back </subtitle>

Journal Articles

Dysregulation of Insulin Secretion in Children With Congenital Hyperinsulinism due to Sulfonylurea Receptor Mutations

A. Grimberg, R.J. Ferry, Jr., A. Kelly, S. Koo-McCoy, K. Polonsky, B. Glaser, M.A. Permutt, L. Aguilar-Bryan, D. Stafford, P.S. Thornton, L. Baker, Charles A. Stanley

Diabetes 2001;50(2):322–328

https://doi.org/10.2337/diabetes.50.2.322

Published: 01 February 2001

View article titled, Dysregulation of Insulin Secretion in Children With Congenital Hyperinsulinism due to Sulfonylurea Receptor Mutations

Journal Articles

A Nonsense Mutation in the Inward Rectifier Potassium Channel Gene, Kir6.2, Is Associated With Familial Hyperinsulinism

Ann Nestorowicz, Nobuya Inagaki, Tohru Gonoi, Kathleen P Schoor, Beth Anne Wilson, Benjamin Glaser, Heddy Landau, Charles A Stanley, Paul S Thornton, Susumu Seino, M Alan Permutt

Diabetes 1997;46(11):1743–1748

https://doi.org/10.2337/diab.46.11.1743

Published: 01 November 1997

View article titled, A Nonsense Mutation in the Inward Rectifier Potassium Channel Gene, Kir6.2, Is Associated With Familial Hyperinsulinism

NARROW

Phenotypic Characterization of Congenital Hyperinsulinism Due to Novel Activating Glucokinase Mutations

Functional Maturation of Pancreatic ß Cells during Development

Regulation of K_ATP Channel Trafficking in Pancreatic β-Cells by Protein Histidine Phosphorylation

Functional and Metabolomic Consequences of K_ATP Channel Inactivation in Human Islets

GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Fasting Blood Glucose Levels in Congenital Hyperinsulinism Owing to Inactivating Mutations in the ATP-Sensitive K⁺ Channel

Diazoxide-Unresponsive Congenital Hyperinsulinism in Children With Dominant Mutations of the β-Cell Sulfonylurea Receptor SUR1

Extremes of Clinical and Enzymatic Phenotypes in Children With Hyperinsulinism Caused by Glucokinase Activating Mutations

Follow-Up Analysis of Genome-Wide Association Data Identifies Novel Loci for Type 1 Diabetes

A Novel Susceptibility Locus for Type 1 Diabetes on Chr12q13 Identified by a Genome-Wide Association Study

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

A Mutation in the TMD0-L0 Region of Sulfonylurea Receptor-1 (L225P) Causes Permanent Neonatal Diabetes Mellitus (PNDM)

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

Glutaminolysis and Insulin Secretion: From Bedside to Bench and Back

Dysregulation of Insulin Secretion in Children With Congenital Hyperinsulinism due to Sulfonylurea Receptor Mutations

A Nonsense Mutation in the Inward Rectifier Potassium Channel Gene, Kir6.2, Is Associated With Familial Hyperinsulinism

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