ArticleMolecular medicine reports2018
Bidirectional modulation of insulin action by reactive oxygen species in 3T3‑L1 adipocytes.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 18 citations in OpenAlex.
- Nidulin stimulates glucose uptake in myotubes through the IRS-AKT pathway and alters redox balance and intracellular calcium.Natural products and bioprospecting · 2025Article
- Comparing Methods for Induction of Insulin Resistance in Mouse 3T3-L1 Cells.Current diabetes reviews · 2025Article
- Multiple Direct Effects of the Dietary ProtoalkaloidNutrients · 2022Article
- Complexity of NAC Action as an Antidiabetic Agent: Opposing Effects of Oxidative and Reductive Stress on Insulin Secretion and Insulin Signaling.International journal of molecular sciences · 2022Article
- High-fat diet-induced obesity and impairment of brain neurotransmitter pool.Translational neuroscience · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) serve an important role in glucose‑lipid metabolic regulation. In the present study, the results demonstrated that there was bidirectional regulation of insulin action in 3T3‑L1 adipocytes treated with ROS. Transient and acute ROS exposure improved insulin‑induced metabolic effects in 3T3‑L1 adipocytes. Hydrogen peroxide (H2O2), as a stable and diffusible ROS, diffused into adipocytes and altered intracellular redox homeostasis, resulting in oxidation and inactivation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN). Inactivation of PTEN enhanced the activation of insulin‑induced protein kinase B (AKT), leading to increased glucose transporter 4 (GLUT4) redistribution and glucose uptake in 3T3‑L1 adipocytes. However, chronic ROS treatment induced insulin resistance in 3T3‑L1 adipocytes. It was also revealed that insulin‑induced AKT activation, GLUT4 translocation to cell membrane and glucose uptake were significantly inhibited in chronic ROS‑treated 3T3‑L1 adipocytes. Taken together, the present study provided further demonstration that transient ROS treatment improved insulin sensitivity; however, chronic ROS exposure induced insulin resistance in 3T3‑L1 adipocytes.
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Registered trials
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