Vitisin A inhibits adipocyte differentiation through cell cycle arrest in 3T3-L1 cells

• Published in: Biochemical and biophysical research communications Vol. 372; no. 1; pp. 108 - 113
• Main Authors: Kim, Soon-hee, Park, Hee-Sook, Lee, Myoung-su, Cho, Yong-Jin, Kim, Young-Sup, Hwang, Jin-Taek, Sung, Mi Jeong, Kim, Myung Sunny, Kwon, Dae Young
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 18-07-2008
• Subjects: 3T3-L1 Cells; 60 APPLIED LIFE SCIENCES; Adipocyte differentiation; Adipocytes - drug effects; Adipogenesis - drug effects; Animals; Anti-Obesity Agents - pharmacology; Benzofurans - pharmacology; CELL CYCLE; Cell cycle arrest; Cell Proliferation - drug effects; Cyclin-Dependent Kinase Inhibitor p21 - metabolism; INHIBITION; METABOLIC DISEASES; Mice; Mitosis - drug effects; MONOCLINIC LATTICES; PHASE TRANSFORMATIONS; Phenols - pharmacology; PHOSPHORUS 21; PHOSPHORYLATION; Phosphorylation - drug effects; PPAR gamma - antagonists & inhibitors; PROLIFERATION; Retinoblastoma Protein - metabolism; Signal Transduction - drug effects; STILBENE; Stilbenes - pharmacology; TRANSCRIPTION; Transcription, Genetic - drug effects; Vitisin A; Cell cycle arrest; Adipocyte differentiation; Proliferation; Vitisin A
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2008.04.188

Inhibition of adipocyte differentiation is one approach among the anti-obesity strategies. This study demonstrates that vitisin A, a resveratrol tetramer, inhibits adipocyte differentiation most effectively of 18 stilbenes tested. Fat accumulation and PPARγ expression were decreased by vitisin A in a dose-dependent manner. Vitisin A significantly inhibited preadipocyte proliferation and consequent differentiation within the first 2
days of treatment, indicating that the anti-adipogenic effect of vitisin A was derived from anti-proliferation. Based on cell cycle analysis, vitisin A blocked the cell cycle at the G1-S phase transition, causing cells to remain in the preadipocyte state. Vitisin A increased p21 expression, while the Rb phosphorylation level was reduced. Therefore, vitisin A seems to induce G1 arrest through p21- and consequent Rb-dependent suppression of transcription. On the other hand, ERK and Akt signaling pathways were not involved in the anti-mitotic regulation by vitisin A. Taken together, these results suggest that vitisin A inhibits adipocyte differentiation through preadipocyte cell cycle arrest.