Data in Brief (Sep 2015)

Data in support of fumosorinone, a novel PTP1B inhibitor, activates insulin signaling in insulin-resistance HepG2 cells and shows anti-diabetic effect in diabetic KKAy mice

  • Du-Qiang Luo,
  • Zhi-Qin Liu,
  • Ting Liu,
  • Chuan Chen,
  • Ming-Yan Li,
  • Zi-Yu Wang,
  • Ruo-song Chen,
  • Gui-xiang Wei,
  • Xiao-yi Wang

DOI
https://doi.org/10.1016/j.dib.2015.03.006
Journal volume & issue
Vol. 4, no. C
pp. 159 – 161

Abstract

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This data article contains data related to the research article entitled “Fumosorinone, a novel PTP1B inhibitor, activates insulin signaling in insulin-resistance HepG2 cells and shows anti-diabetic effect in diabetic KKAy mice” in the Toxicology and Applied Pharmacology [1]. Fumosorinone (FU) is a new inhibitor of protein phosphatase 1B inhibitor, which was isolated from insect pathogenic fungi Isaria fumosorosea. FU was found to inhibit PTP1B activity in our previous study [2]. PTP1B is the physiological antagonist of the insulin signalling pathway. Inhibition of PTP 1B may increase insulin sensitivity [3]. PTP1B has been considered promising as an insulin-sensitive drug target for the prevention and the treatment of insulin-based diseases [4]. We determined the effect of FU on the glucose consumption of IR HepG2 cells. FU caused significant enhancement in glucose consumption by insulin-resistant HepG2 cells compared with control cells.