Physiologically achievable doses of resveratrol enhance 3T3-L1 adipocyte differentiation
Abstract
Purpose Resveratrol is a natural polyphenolic stilbene widely found in grapes, berries, and other plants. Caloric restriction-like effects of resveratrol have been associated with suppressive and apoptotic effects on adipocyte differentiation in vitro when used at high doses (≥ 20 µM), which may not be achievable in vivo. The aim of this study was to investigate the effects of resveratrol at physiologically achievable low doses (1 and 10 μM) on 3T3-L1 adipocyte differentiation.Methods 3T3-L1 preadipocytes were differentiated into adipocytes using a modified adipogenic cocktail in the presence or absence of resveratrol. Differentiation was determined by lipid accumulation and mRNA expression of marker genes. Activation of glucocorticoid receptor (GR) and peroxisome proliferator-activated receptor γ (PPARγ) was determined by transcription factor-mediated reporter assays and mRNA expression of target genes. Protein samples were collected for the study of AMPK activation.Results Resveratrol at physiologically achievable doses (1 and 10 µM) significantly enhanced 3T3-L1 adipocyte differentiation although the effect was less pronounced compared with that achieved under optimal differentiation cocktail in vitro. Resveratrol (1-50 µM) dose dependently activated or synergized with the synthetic ligand or adipogenic treatment to activate GR and PPARγ. However, resveratrol induced cell death when used at doses above 10 µM in differentiating cells.Conclusions Our results report for the first time that resveratrol at physiologically achievable doses (1 and 10 µM) enhances 3T3-L1 adipocyte differentiation, which supports the emerging paradigm that enhanced adipocyte differentiation may be associated with caloric restriction-like metabolic effects for resveratrol.
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Hu et al. reported dose-dependent stimulation of adipocyte differentiation at resveratrol concentrations of 1 and 10 μM, and an inhibitory effect at 50 and 100 μM, confirmed by reduction in C/EBPα, FABP4, and PPARγ.
“The author reported a dose-dependent stimulation of adipocytes differentiation at concentrations of 1 and 10 μM. Conversely, an inhibitory effect was found at concentrations of 50 and 100 μM, as confirmed by the reduction in the expression of C/EBPα, FABP4, and PPARγ.”
From The Role of Resveratrol Administration in Human Obesity (2021) · cites this paper as [29]
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Self-citation
- Authors
- Hu, P., Zhao, L., & Chen, J.
- Affiliations
- University of Tennessee at Knoxville (US)
- Corresponding author
- Chen, Jiangang
- Venue
- European Journal of Nutrition
- Published
- 2014-07-17
- Volume
- 54
- Issue
- 4
- Pages
- 569-579
- ISSN
- 1436-6207 (ISSN-L)
- 1436-6215
- OpenAlex
- W2135149765
- Cited by
- 35
- References
- 45
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 4 · 2014: 2
- FWCI
- 2.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- European Journal of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Syddansk Universitet
- National Institutes of Health (5r21es017475-02)
- National Institute of Environmental Health Sciences (R21 ES017475, 1R21ES017475-01A1)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R24HD042854)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- resveratrol, adipogenesis, 3T3-L1 preadipocytes, glucocorticoid receptor, PPARγ, AMPK activation, polyphenols, cell death
- MeSH terms
- Resveratrol, Animals, Cell Differentiation, Dose-Response Relationship, Drug, Receptors, Glucocorticoid, RNA, Messenger, Stilbenes, Transcription Factors, Adipocytes, RNA, Small Interfering, 3T3-L1 Cells, PPAR gamma, Mice
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