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Methotrexate enhances 3T3-L1 adipocytes hypertrophy
Cláudia Marques1, Diana Teixeira, Ana Cunha
1Departamento de Bioquímica (U38-FCT), Faculdade de Medicina, Universidade do Porto, Alameda Prof. Hernâni Monteiro, 4200-319, Oporto, Portugal. csmarques@med.up.pt
Methotrexate (MTX) impacts fat cell growth and function. This study shows MTX affects preadipocyte proliferation and adipogenesis, potentially influencing metabolic health in rheumatoid arthritis patients.
Area of Science:
- Cell Biology
- Metabolism
- Pharmacology
Background:
- Methotrexate (MTX) is a common treatment for rheumatoid arthritis (RA).
- Metabolic syndrome (MeS) is prevalent in RA patients.
- Adipose tissue plays a key role in metabolic complications.
Purpose of the Study:
- To investigate the effects of MTX on preadipocyte proliferation.
- To assess MTX's impact on adipogenesis (fat cell differentiation).
- To determine MTX's influence on glucose uptake by adipocytes.
Main Methods:
- Used 3T3-L1 preadipocytes.
- Assessed proliferation via sulforhodamine B staining and (3H)-thymidine incorporation.
- Evaluated adipogenesis by Oil Red O staining for lipid accumulation.
- Measured glucose uptake using (3H)-deoxyglucose ((3H)-DG) uptake assays.
Main Results:
- MTX reduced preadipocyte proliferation and protein content in a dose-dependent manner.
- Low-dose MTX (0.1 μM) enhanced lipid accumulation and basal glucose uptake in adipocytes.
- MTX-treated adipocytes showed impaired insulin-stimulated glucose uptake.
Conclusions:
- Methotrexate interferes with adipocyte proliferation and promotes hypertrophic growth.
- MTX alters adipocyte function, affecting lipid accumulation and glucose metabolism.
- These findings suggest potential implications for the metabolic profile of RA patients undergoing MTX treatment.
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