Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells

Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells

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...

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Autores principales: Blaise Su Jun Low, Chang Siang Lim, Shirley Suet Lee Ding, Yaw Sing Tan, Natasha Hui Jin Ng, Vidhya Gomathi Krishnan, Su Fen Ang, Claire Wen Ying Neo, Chandra S. Verma, Shawn Hoon, Su Chi Lim, E. Shyong Tai, Adrian Kee Keong Teo
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/03229c3f34e24347bae20e13a756621c
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Sumario: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.

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