Nature Communications (May 2021)

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

  • 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

DOI
https://doi.org/10.1038/s41467-021-22843-4
Journal volume & issue
Vol. 12, no. 1
pp. 1 – 20

Abstract

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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.