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AIM: To investigate the influence of C75, a fatty acid synthase inhibitor, on adipocyte differentiation. METHODS: Mouse 3T3-L1 preadipocytes were induced to differentiation by insulin, isobutylmethylxanthine, and dexamethasone. Oil red O staining was performed and activity of glycerol-3-phosphate dehydrogenase (GPDH) was measured. The level of peroxisome proliferators-activated receptor y (PPARy) mRNA was assayed by semi-quantitative reverse transcription PCR. RESULTS: C75 blocked the adipogenic conversion in a dose-dependent manner and the inhibitory effects occurred both in the early phases (48 h) and in the latter phases (8 d) of the process. Treatment with C75 for 8 d induced more decrease in lipid content than 48 h (P<0.01). Treatment with C75 50 mg/L for 48 h or 8 d decreased GPDH activity by 52.8 % and 31.2 % of Vehicle, respectively. Treatment with C75 10-50 mg/L for 48 h or 8 d down-regulated PPARy mRNA expression compared with control (P<0.01). CONCLUSION: C75 blocked the adipocyte differentiat
AIM: To investigate the influence of C75, a fatty acid synthase inhibitor, on adipocyte differentiation. METHODS: Mouse 3T3-L1 preadipocytes were induced to differentiation by insulin, isobutylmethylxanthine, and dexamethasone. Oil red O staining was performed and activity of glycerol-3 The level of peroxisome proliferators-activated receptor y (PPARy) mRNA was assayed by semi-quantitative reverse transcription PCR. RESULTS: C75 blocked the adipogenic conversion in a dose-dependent manner and inhibitory effects. Treatment with C75 for 8 d induced more decrease in lipid content than 48 h (P <0.01). Treatment with C75 50 mg / L for 48 h or 8 d decreased GPDH activity by 52.8% and 31.2% of Vehicle, respectively. Treatment with C75 10-50 mg / L for 48 h or 8 d down-regulated PPARy mRNA expression compared with control (P <0.01). CONCLUSION: C75 blocked the adi pocyte differentiat