ArticlePloS one2013
Prolonged induction activates Cebpα independent adipogenesis in NIH/3T3 cells.
Article in PloS one, 2013. 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, 13 citations in OpenAlex.
- Article
- Article
- An intronic enhancer of Cebpa regulates adipocyte differentiation and adipose tissue development via long-range loop formation.Cell proliferation · 2024Article
- Lotus (Nutrients · 2022Article
- Bilobalide Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway.Molecules (Basel, Switzerland) · 2019Article
- Stable and reproducible transgene expression independent of proliferative or differentiated state using BAC TG-EMBED.Gene therapy · 2018Article
- MicroRNA-142a-3p promotes the differentiation of 3T3-L1 preadipocytes by targeting high-mobility group AT-hook 1.International journal of clinical and experimental pathology · 2018Article
- CCAAT/enhancer binding protein β in relation to ER stress, inflammation, and metabolic disturbances.BioMed research international · 2015Review
- N-Acetylcysteine affects obesity-related protein expression in 3T3-L1 adipocytes.Redox report : communications in free radical research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background3T3-L1 cells are widely used to study adipogenesis and insulin response. Their adipogenic potential decreases with time in the culture. Expressing exogenous genes in 3T3-L1 cells can be challenging. This work tries to establish and characterize an alternative model of cultured adipocytes that is easier to work with than the 3T3-L1 cells. METHODOLOGY/PRINCIPAL
findingsINDUCED CELLS WERE IDENTIFIED AS ADIPOCYTES BASED ON THE FOLLOWING THREE CHARACTERISTICS: (1) Accumulation of triglyceride droplets as demonstrated by oil red O stain. (2) Transport rate of 2-deoxyglucose increased after insulin stimulation. (3) Expression of fat specific genes such as Fabp4 (aP2), Slc2a4 (Glut4) and Pparg (PPARγ). Among the cell lines induced under different conditions in this study, only NIH/3T3 cells differentiated into adipocytes after prolonged incubation in 3T3-L1 induction medium containing 20% instead of 10% fetal bovine serum. Rosiglitazone added to the induction medium shortened the incubation period from 14 to 7 days. The PI3K/AKT pathway showed similar changes upon insulin stimulation in these two adipocytes. C/EBPα mRNA was barely detectable in NIH/3T3 adipocytes. NIH/3T3 adipocytes induced in the presence of rosiglitazone showed higher 2-deoxyglucose transport rate after insulin stimulation, expressed less Agt (angiotensinogen) and more PPARγ. Knockdown of C/EBPα using shRNA blocked 3T3-L1 but not NIH/3T3 cell differentiation. Mouse adipose tissues from various anatomical locations showed comparable levels of C/EBPα mRNA. CONCLUSIONS/SIGNIFICANCE: NIH/3T3 cells were capable of differentiating into adipocytes without genetic engineering. They were an adipocyte model that did not require the reciprocal activation between C/EBPα and PPARγ to differentiate. Future studies in the C/EBPα independent pathways leading to insulin responsiveness may reveal new targets to diabetes treatment.
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