ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021
A-FABP-PTEN/AKT Regulates Insulin Resistance in Preadipocyte Cell 3T3-L1 Cells.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Reversing diastolic dysfunction in diabetes: a mitochondrial quality control-centric pharmacological approach.Acta diabetologica · 2026Review
- Neferine inhibits vascular smooth muscle cell proliferation and migration in atherosclerosis by targeting CYS130 and PHE252 in PTEN.Frontiers in pharmacology · 2026Article
- Signaling Pathways Related to Oxidative Stress in Diabetic Cardiomyopathy.Frontiers in endocrinology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe purpose of this study was to explore the regulation of A-FABP-PTEN/AKT on insulin resistance in preadipocyte 3T3-L1 cell.
methodssiRNA interference method was used to knock-down the A-FABP expression in 3T3-L1 cells. The cell proliferation was detected by oil-O staining and MTT. The protein and mRNA expression levels of A-FABP, PTEN and AKT were detected by Western blot and qPCR.
resultsInhibition of A-FABP expression increased cell proliferation activity of the 3T3-L1 cells. Moreover, siRNA3 significantly reduced A-FABP mRNA expression compared with siRNA1 and siRNA2 (
conclusionOur finding suggested that A-FABP can directly inhibit the phosphorylation of AKT and increase the PTEN expression in the process of normal adipocyte differentiation, which speculated that A-FABP played a crucial role by adjusting the AKT activity in the process of adipocyte differentiation.
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Registered trials
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