Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells
Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived huma...
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| Published in | Nature communications Vol. 12; no. 1; pp. 3133 - 20 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
25.05.2021
Nature Publishing Group Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-1723 2041-1723 |
| DOI | 10.1038/s41467-021-22843-4 |
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| Abstract | Heterozygous
HNF1A
gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal
HNF1A
+/H126D
mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating
GLUT2
and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients.
Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding. |
|---|---|
| AbstractList | Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding. Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal HNF1A +/H126D mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating GLUT2 and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients. Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal HNF1A +/H126D mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating GLUT2 and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients. Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding. Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal HNF1A+/H126D mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating GLUT2 and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients.Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal HNF1A+/H126D mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating GLUT2 and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients. Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific mechanisms of MODY3 in humans remain unclear due to lack of access to diseased human pancreatic cells. Here, we utilize MODY3 patient-derived human induced pluripotent stem cells (hiPSCs) to study the effect(s) of a causal HNF1A+/H126D mutation on pancreatic function. Molecular dynamics simulations predict that the H126D mutation could compromise DNA binding and gene target transcription. Genome-wide RNA-Seq and ChIP-Seq analyses on MODY3 hiPSC-derived endocrine progenitors reveal numerous HNF1A gene targets affected by the mutation. We find decreased glucose transporter GLUT2 expression, which is associated with reduced glucose uptake and ATP production in the MODY3 hiPSC-derived β-like cells. Overall, our findings reveal the importance of HNF1A in regulating GLUT2 and several genes involved in insulin secretion that can account for the insulin secretory defect clinically observed in MODY3 patients.Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show that MODY3-related HNF1A mutation in patient hiPSCderived pancreatic cells decreases glucose transporter GLUT2 expression due to compromised DNA binding. |
| ArticleNumber | 3133 |
| Author | Lim, Chang Siang Tai, E. Shyong Verma, Chandra S. Low, Blaise Su Jun Tan, Yaw Sing Ng, Natasha Hui Jin Neo, Claire Wen Ying Krishnan, Vidhya Gomathi Hoon, Shawn Lim, Su Chi Teo, Adrian Kee Keong Ding, Shirley Suet Lee Ang, Su Fen |
| Author_xml | – sequence: 1 givenname: Blaise Su Jun orcidid: 0000-0003-3304-0861 surname: Low fullname: Low, Blaise Su Jun organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR), Yong Loo Lin School of Medicine, National University of Singapore – sequence: 2 givenname: Chang Siang orcidid: 0000-0001-9818-6058 surname: Lim fullname: Lim, Chang Siang organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR), Saw Swee Hock School of Public Health, National University of Singapore – sequence: 3 givenname: Shirley Suet Lee surname: Ding fullname: Ding, Shirley Suet Lee organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR) – sequence: 4 givenname: Yaw Sing orcidid: 0000-0002-2522-9421 surname: Tan fullname: Tan, Yaw Sing organization: Bioinformatics Institute, Agency for Science, Technology and Research (ASTAR) – sequence: 5 givenname: Natasha Hui Jin surname: Ng fullname: Ng, Natasha Hui Jin organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR) – sequence: 6 givenname: Vidhya Gomathi surname: Krishnan fullname: Krishnan, Vidhya Gomathi organization: Molecular Engineering Lab (MEL), IMCB, ASTAR – sequence: 7 givenname: Su Fen surname: Ang fullname: Ang, Su Fen organization: Khoo Teck Puat Hospital – sequence: 8 givenname: Claire Wen Ying surname: Neo fullname: Neo, Claire Wen Ying organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR), Yong Loo Lin School of Medicine, National University of Singapore – sequence: 9 givenname: Chandra S. surname: Verma fullname: Verma, Chandra S. organization: Bioinformatics Institute, Agency for Science, Technology and Research (ASTAR), Department of Biological Sciences, National University of Singapore, School of Biological Sciences, Nanyang Technological University – sequence: 10 givenname: Shawn orcidid: 0000-0002-3892-3332 surname: Hoon fullname: Hoon, Shawn organization: Molecular Engineering Lab (MEL), IMCB, ASTAR – sequence: 11 givenname: Su Chi surname: Lim fullname: Lim, Su Chi organization: Saw Swee Hock School of Public Health, National University of Singapore, Khoo Teck Puat Hospital – sequence: 12 givenname: E. Shyong surname: Tai fullname: Tai, E. Shyong organization: Yong Loo Lin School of Medicine, National University of Singapore – sequence: 13 givenname: Adrian Kee Keong orcidid: 0000-0001-5901-7075 surname: Teo fullname: Teo, Adrian Kee Keong email: ateo@imcb.a-star.edu.sg organization: Stem Cells and Diabetes Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (ASTAR), Yong Loo Lin School of Medicine, National University of Singapore |
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| Snippet | Heterozygous
HNF1A
gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific... Heterozygous HNF1A gene mutations can cause maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. However, specific... Heterozygous HNF1A mutations can give rise to maturity onset diabetes of the young 3 (MODY3), characterized by insulin secretion defects. Here the authors show... |
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| SubjectTerms | 13/100 38/91 631/532/1360 631/532/2064/2158 692/163/2743 692/699/2743/137 Beta cells Binding Defects Deoxyribonucleic acid Diabetes Diabetes mellitus DNA Gene expression Genomes Glucose Glucose transporter HNF1a gene Humanities and Social Sciences Insulin Insulin secretion Molecular dynamics multidisciplinary Mutation Pancreas Pluripotency Science Science (multidisciplinary) Secretion Stem cells Transcription |
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| Title | Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells |
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