ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2025
Establishment and Evaluation of HepG2 Cell Insulin Resistance Model.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- DPP-4 inhibitory and insulin-signaling-modulating potential ofFood science and biotechnology · 2026Article
- Article
- Ultrasound-Assisted Ionic Liquid Extraction, Macroporous Resin Purification, and Hypoglycemic Effects of Total Flavonoids fromMolecules (Basel, Switzerland) · 2026Article
- Metabolic and Signaling Dysregulation in a Cellular Model of Hepatic Insulin Resistance.Current issues in molecular biology · 2026Article
- LncRNA MALAT1 drives diabetic kidney injury via Nrf2 suppression in glomerular endothelium.Scientific reports · 2026Article
- Physicochemical Characterization and In Vitro Hypoglycemic Activity of a Low-Molecular-Weight Extracellular Polysaccharide From Deep-Sea Beauveria bassiana.Chemistry & biodiversity · 2026Article
- A Standardized Onion Peel-Derived Bioactive Ingredient Attenuates Palmitate-Induced Steatosis and Oxidative Stress by Modulating Mitochondrial Dynamics and Autophagy in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Natural Extract Combination Modulates Intestinal Barrier and Hepatic Cholesterol via the Gut-Liver Axis In Vitro.Pharmaceutics · 2026Article
- Optimization of Indole- and Pyrazole-fused Glycyrrhetinic Acid Derivatives as Potent PTP1B Inhibitors: In Silico, In Vitro, In Vivo, and Metabolomic Studies.ACS bio & med chem Au · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Establishing HepG2 cell insulin resistance models using glucosamine, high glucose with high insulin and palmitic acid and briefly evaluating them to provide reliable models for insulin resistance research. Methods: Three methods were used to induce insulin resistance in HepG2 cells, and glucose uptake and consumption, glucose metabolism-related mRNA and p-AKT/AKT protein levels and RNA-seq were detected to compare the three induction methods. Results: Glucose consumption capacity was reduced after glucosamine and palmitic acid induction and did not change significantly after high glucose with high insulin induction. Glucose uptake capacity was not significantly changed after glucosamine and high glucose with high insulin induction and was reduced after palmitic acid induction. After high insulin stimulation, p-AKT/AKT levels were elevated in glucosamine and high glucose with high insulin induction and did not change significantly in palmitic acid induction. Conclusion: Treatment with 0.2 mM palmitic acid for 24 h is a simple and stable method to induce insulin resistance in HepG2 cells.
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