Oxidovanadium(IV) sulfate-induced glucose uptake in HepG2 cells through IR/Akt pathway and hydroxyl radicals

Qian Zhao1, Deliang Chen1, Pingsheng Liu2

  • 1Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, No. 19A YuQuan Road, Beijing 100049, China.

Insights

Oxidovanadium(IV) sulfate (VOSO4) enhances glucose uptake by increasing reactive oxygen species (ROS), specifically hydroxyl radicals. This mechanism involves the insulin receptor (IR)/Akt signaling pathway, offering insights into vanadium

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Vanadium compounds exhibit insulin-mimetic and anti-diabetic properties.
  • The precise molecular mechanisms linking vanadium to insulin signaling in diabetes remain unclear.

Purpose of the Study:

  • To investigate the effects of oxidovanadium(IV) sulfate (VOSO4) on glucose uptake and insulin signaling.
  • To elucidate the role of reactive oxygen species (ROS) in VOSO4-induced effects.

Main Methods:

  • Utilized human hepatoma HepG2 cells.
  • Assessed glucose uptake, insulin receptor (IR) and protein kinase B (Akt) phosphorylation, and intracellular ROS generation.
  • Employed Western blot analysis and specific radical scavengers (catalase, sodium formate, superoxide dismutase).

Main Results:

  • VOSO4 treatment (5-50 μM) increased glucose uptake, IR/Akt phosphorylation, and ROS generation.
  • Catalase and sodium formate inhibited hydroxyl radical (·OH) generation and VOSO4-induced IR/Akt phosphorylation.
  • Superoxide dismutase did not affect these VOSO4-induced changes.

Conclusions:

  • VOSO4-induced hydroxyl radicals act as signaling molecules.
  • ·OH radicals promote glucose uptake through the IR/Akt signaling pathway.
  • These findings contribute to understanding vanadium's anti-diabetic mechanisms.

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