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Author Spotlight: High-Throughput Measurement of Intracellular ROS Levels in Hepatocellular Lines
Published on: January 19, 2024
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.
Abstract:
The insulin-mimetic and anti-diabetic properties of vanadium and related compounds have been well documented both in vitro and in vivo. However, the molecular basis of the link between vanadium and the insulin signaling pathway in diabetes mellitus is not fully described. We investigated the effects of reactive oxygen species (ROS) induced by oxidovanadium(IV) sulfate (VOSO4) on glucose uptake and the insulin signaling pathway in human hepatoma cell line HepG2. Exposure of cells to VOSO4 (5-50 μM) resulted in an increase in glucose uptake, insulin receptor (IR) and protein kinase B (Akt) phosphorylation and intracellular ROS generation. Using Western blot, we found that catalase and sodium formate, but not superoxide dismutase, prevented the increase of hydroxyl radical (·OH) generation and significantly decreased VOSO4-induced IR and Akt phosphorylation. These results suggest that VOSO4-induced ·OH radical, which is a signaling species, promotes glucose uptake via the IR/Akt signaling pathway.
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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