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Maturity‐onset diabetes of the young ( MODY ) is a heterozygous monogenic diabetes; more than 13 disease genes have been identified. However, the pathogenesis of  MODY  is not fully understood, because the pancreatic β‐cells of the patients are inaccessable. Therefore, we attempted to establish  MODY  patient‐derived induced pluripotent stem cells ( MODY ‐ iPS ) cells to investigate the pathogenic mechanism of  MODY  by inducing pancreatic β‐cells. We established  MODY 5‐ iPS  cells from a Japanese patient with  MODY 5 (R177X), and confirmed that  MODY 5‐ iPS  cells possessed the characteristics of pluripotent stem cells. In the course of differentiation from  MODY 5‐ iPS  cells into pancreatic β‐cells, we examined the disease gene,   HNF 1B  messenger ribonucleic acid. We found that the amount of R177X mutant transcripts was much less than that of wild ones, but they increased after adding cycloheximide to the medium. These results suggest that these R177X mutant messenger ribonucleic acids are disrupted by nonsense‐mediated messenger ribonucleic acid decay in  MODY ‐ iPS  cells during the developmental stages of pancreatic β‐cells.

Establishment of maturity‐onset diabetes of the young‐induced pluripotent stem cells from a Japanese patient