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Quercetin exerts anti‐adipogenic effects through modulation of 3T3‐L1 preadipocyte proliferation and differentiation
Author(s) -
Swick Jennifer,
Lee Ok Hwan,
Kim Young-Cheul
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.644.11
Subject(s) - adipogenesis , quercetin , cell cycle , 3t3 l1 , microbiology and biotechnology , lipid droplet , endocrinology , medicine , peroxisome proliferator activated receptor , chemistry , biology , cell , adipose tissue , biochemistry , receptor , antioxidant
Obesity is a strong risk factor for the development of diabetes, cardiovascular disease, and cancer. At the cellular level, obesity is characterized by differentiation of preadipocytes into an excessive number of adipocytes; a process tightly regulated by cell cycle events and adipogenic transcription regulators. We investigate the mechanisms by which quercetin, the most commonly consumed dietary flavonoid, regulates adipogenesis. 3T3‐L1 preadipocytes were differentiated with or without quercetin treatment. The changes in lipid accumulation, and gene expression related to cell cycle and adipogenesis were assessed. Quercetin between 10–100μM dose‐dependently inhibited mRNA expression of PPARγ and C/EBPα. Quercetin at 50μM also significantly inhibited PPARγ protein expression, suggesting the inhibitory effects at both transcriptional and translational levels. Cells treated with 50μM quercetin between 0 and 36 hrs, the early phase of mitotic clonal expansion (MCE), exhibited a significant decrease in lipid accumulation. However, there was no inhibitory effect in the cells treated on days 2 and 3. Furthermore, quercetin at 50μM suppressed mRNA expression of Cyclin A, a key regulator of cell cycle entry into S phase between 12 and 24 hrs. These results suggest quercetin suppresses adipogenesis by inhibiting the early MCE phase required for induction of adipogenic factors and terminal differentiation.