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Retraction Free access | 10.1172/JCI92775

iPSC-derived β cells model diabetes due to glucokinase deficiency

Haiqing Hua, Linshan Shang, Hector Martinez, Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K. Chung, Robin Goland, Rudolph L. Leibel, and Dieter Egli

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Published January 17, 2017 - More info

Published in Volume 127, Issue 3 on March 1, 2017
J Clin Invest. 2017;127(3):1115–1115. https://doi.org/10.1172/JCI92775.
Copyright © 2017, American Society for Clinical Investigation
Published January 17, 2017 - Version history
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iPSC-derived β cells model diabetes due to glucokinase deficiency
Haiqing Hua, … , Rudolph L. Leibel, Dieter Egli
Haiqing Hua, … , Rudolph L. Leibel, Dieter Egli
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iPSC-derived β cells model diabetes due to glucokinase deficiency

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Abstract

Diabetes is a disorder characterized by loss of β cell mass and/or β cell function, leading to deficiency of insulin relative to metabolic need. To determine whether stem cell–derived β cells recapitulate molecular-physiological phenotypes of a diabetic subject, we generated induced pluripotent stem cells (iPSCs) from subjects with maturity-onset diabetes of the young type 2 (MODY2), which is characterized by heterozygous loss of function of the gene encoding glucokinase (GCK). These stem cells differentiated into β cells with efficiency comparable to that of controls and expressed markers of mature β cells, including urocortin-3 and zinc transporter 8, upon transplantation into mice. While insulin secretion in response to arginine or other secretagogues was identical to that in cells from healthy controls, GCK mutant β cells required higher glucose levels to stimulate insulin secretion. Importantly, this glucose-specific phenotype was fully reverted upon gene sequence correction by homologous recombination. Our results demonstrate that iPSC-derived β cells reflect β cell–autonomous phenotypes of MODY2 subjects, providing a platform for mechanistic analysis of specific genotypes on β cell function.

Authors

Haiqing Hua, Linshan Shang, Hector Martinez, Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K. Chung, Robin Goland, Rudolph L. Leibel, Dieter Egli

×

Original citation: J Clin Invest. 2013;123(7):3146–3153. https://doi.org/10.1172/JCI67638

Citation for this retraction: J Clin Invest. 2017;127(3):1115. https://doi.org/10.1172/JCI92775

The corresponding authors were made aware of karyotype abnormalities through a routine quality control test of pluripotent stem cells used in the studies reported in this paper. After extensive internal review and genetic analysis, they found that the karyotypes of some of the cells used for the experiments reported were abnormal and that the normal karyotypes shown in Figure 1 and Supplemental Figure 2 were not from cell lines used in the study. They also cannot confirm the endonuclease-mediated correction of the mutant GCK G299R allele. H. Hua takes responsibility for the characterization and presentation of cell line karyotypes and the genetic manipulations. Because of these discrepancies, the authors wish to retract the article. They apologize for these errors and for any inconvenience caused to others.

Footnotes

See the related article at iPSC-derived β cells model diabetes due to glucokinase deficiency.

Version history
  • Version 1 (January 17, 2017): Electronic publication
  • Version 2 (March 1, 2017): Print issue publication

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