Sulforaphane inhibits mitotic clonal expansion during adipogenesis through cell cycle arrest
Choi KM, Lee YS, Sin DM, Lee S, Lee MK, Lee YM, Hong JT, Yun YP, Yoo HS
Obesity (Silver Spring, Md.) · 72 citas
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Solo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
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- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Universidad u hospital
- Chungbuk National University
Según 1 financiador declarado.
Publicación
- Publicado
- 2012-01-26 · Obesity (Silver Spring) · vol. 20 · número 7 · págs. 1365–1371
- Editorial
- Wiley
- Citado
- 95 citas · más que el 91% de estudios similares · 2.8× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 42 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Retinoids in leukemia and cellular processes · Immune Cell Function and Interaction
- Palabras clave
- Sulforaphane, Adipogenesis, Adipocyte, Internal medicine, Endocrinology, Chemistry, Cell cycle, Biology, Cell biology, Cell, Biochemistry, Medicine, Adipose tissue
- MeSH
- cell line, 3t3-l1 cells, adipocytes, animals, humans, mice, rats, thiocyanates, isothiocyanates, sulfoxides, proliferating cell nuclear antigen, ppar gamma, transcription factors, anticarcinogenic agents, blotting, western, mitosis, cell differentiation, cell proliferation, up-regulation, adipogenesis, cell cycle checkpoints
9 autores
- Kyeong‐Mi Choi🇰🇷Chungbuk National University
- Youn‐Sun Lee🇰🇷Chungbuk National University
- Dong‐Mi Sin🇰🇷Chungbuk National University
- Seunghyun Lee🇰🇷Chungbuk National University
- Mi Kyeong Lee🇰🇷Chungbuk National University
- Yong‐Moon Lee🇰🇷Chungbuk National University
- Jin‐Tae Hong🇰🇷Chungbuk National University
- Yeo‐Pyo Yun🇰🇷Chungbuk National University
- Hwan‐Soo Yoo🇰🇷 · autor de correspondenciaChungbuk National University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3-L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G(0)/G(1) phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G(0)/G(1) phase through upregulation of p27 expression.
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