Type 2 diabetes and congenital hyperinsulinism cause DNA double-strand breaks and p53 activity in β cells.

@article{TornovskyBabeay2014Type2D,
  title={Type 2 diabetes and congenital hyperinsulinism cause DNA double-strand breaks and p53 activity in β cells.},
  author={Sharona Tornovsky-Babeay and Daniela Dadon and Oren Ziv and Elhanan Tzipilevich and Tehila Kadosh and Rachel Schyr-Ben Haroush and Ayat Hija and Miri Stolovich-Rain and Judith Furth-Lavi and Zvi Granot and S. Ben – Porat and Louis Philipson and Kevan C Herold and Tricia R. Bhatti and Charles A. Stanley and Frances M. Ashcroft and Peter in't Veld and Ann Saada and Mark A Magnuson and Benjamin Glaser and Yuval Dor},
  journal={Cell metabolism},
  year={2014},
  volume={19 1},
  pages={
          109-21
        }
}
β cell failure in type 2 diabetes (T2D) is associated with hyperglycemia, but the mechanisms are not fully understood. Congenital hyperinsulinism caused by glucokinase mutations (GCK-CHI) is associated with β cell replication and apoptosis. Here, we show that genetic activation of β cell glucokinase, initially triggering replication, causes apoptosis associated with DNA double-strand breaks and activation of the tumor suppressor p53. ATP-sensitive potassium channels (KATP channels) and… CONTINUE READING
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