ArticleJournal of translational medicine2024
VEGFB ameliorates insulin resistance in NAFLD via the PI3K/AKT signal pathway.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Review
- Forsythoside A Attenuates High-Fat Diet-Induced Obesity by Regulating Thermogenesis and Browning of White Adipose Tissue Through Activation of the AMPK Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- AIBP deficiency drives MAFLD advancement via ITGβ3 mediated lipid metabolism disruption and pro-inflammatory activation.Cell communication and signaling : CCS · 2026Article
- Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation-A Narrative Review.Biomedicines · 2026Review
- Influence and treatment of insulin receptor substrate/PI3K/Akt‑mediated insulin resistance in diabetes mellitus (Review).Molecular medicine reports · 2026Review
- Daixie recipe ameliorates diet-induced MASH in miceFrontiers in endocrinology · 2026Article
- Association of adherence to the EAT-Lancet diet and risk of uterine cancer: a prospective cohort from the UK Biobank.Frontiers in nutrition · 2026Article
- RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.Cell & bioscience · 2025Article
- Magnesium Promotes Growth-Metabolism Balance in Juvenile Largemouth Bass (Antioxidants (Basel, Switzerland) · 2025Article
- Smilax china L. Polysaccharide Alleviates HFD-induced Insulin Resistance via Modulating Gut Microbiota and AMPK/PI3K/AKT Signaling Pathway in Mice.Plant foods for human nutrition (Dordrecht, Netherlands) · 2025Article
- Ginsenoside Rf improves glucose metabolism via the IRS/PI3K/Akt and PPARα/PGC1α signaling pathways in insulin-resistant AML12 cells.BMC complementary medicine and therapies · 2025Article
- Flavone C-Glycosides fromNutrients · 2025Article
- CSE/HInternational journal of molecular sciences · 2025Review
- Integrated multi-omics analysis reveals the mechanisms of naringin in ameliorating high-fat diet-induced metabolic dysfunction-associated steatotic liver disease.Frontiers in nutrition · 2025Article
- The gut-adipose/pancreas axis: a novel perspective on glycolipid metabolism dysregulation in MAFLD and T2DM pathogenesis.Frontiers in endocrinology · 2025Review
- Metabolic dysregulation in MASLD-associated HCC: diagnostic biomarkers and therapeutic opportunities.Frontiers in medicine · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is one of the most universal liver diseases with complicated pathogenesis throughout the world. Insulin resistance is a leading risk factor that contributes to the development of NAFLD. Vascular endothelial growth factor B (VEGFB) was described by researchers as contributing to regulating lipid metabolic disorders. Here, we investigated VEGFB as a main target to regulate insulin resistance and metabolic syndrome.
methodsIn this study, bioinformatics, transcriptomics, morphological experiments, and molecular biology were used to explore the role of VEGFB in regulating insulin resistance in NAFLD and its molecular mechanism based on human samples, animal models, and cell models. RNA-seq was performed to analyze the signal pathways associated with VEGFB and NAFLD; Palmitic acid and High-fat diet were used to induce insulin-resistant HepG2 cells model and NAFLD animal model. Intracellular glucolipid contents, glucose uptake, hepatic and serum glucose and lipid levels were examined by Microassay and Elisa. Hematoxylin-eosin staining, Oil Red O staining, and Periodic acid-schiff staining were used to analyze the hepatic steatosis, lipid droplet, and glycogen content in the liver. Western blot and quantitative real-time fluorescent PCR were used to verify the expression levels of the VEGFB and insulin resistance-related signals PI3K/AKT pathway.
resultsWe observed that VEGFB is genetically associated with NAFLD and the PI3K/AKT signal pathway. After VEGFB knockout, glucolipids levels were increased, and glucose uptake ability was decreased in insulin-resistant HepG2 cells. Meanwhile, body weight, blood glucose, blood lipids, and hepatic glucose of NAFLD mice were increased, and hepatic glycogen, glucose tolerance, and insulin sensitivity were decreased. Moreover, VEGFB overexpression reduced glucolipids and insulin resistance levels in HepG2 cells. Specifically, VEGFB/VEGFR1 activates the PI3K/AKT signals by activating p-IRS1
conclusionsOur studies suggest that VEGFB could present a novel strategy for treating NAFLD as a positive factor.
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