Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Hwayang-dong 1, Gwangjin-gu, Seoul 143-701, Republic of Korea.
J Nutr Biochem. 2012 Dec;23(12):1552-8. doi: 10.1016/j.jnutbio.2011.10.008. Epub 2012 Mar 8.
Garlic extracts exert anti-cancer and anti-inflammatory effects. However, the anti-adipogenic effect of garlic-derived compounds remains unclear. In this study, we examined the effect of thiacremonone, a sulfur compound isolated from garlic, on adipocyte differentiation using 3T3-L1 cells. We found that thiacremonone significantly inhibited 3T3-L1 differentiation via down-regulation of adipogenesis-related transcription factors and adipogenic markers. The inhibitory effect mainly occurred at the early phase of differentiation in 3T3-L1 cells. There was no cytotoxic effect of thiacremonone in 3T3-L1 cells and treatment of differentiating 3T3-L1 cells with thiacremonone resulted in AMPK activation, which led to an attenuated expression of acetyl CoA carboxylase-1 (ACC-1), an essential enzyme for the synthesis and usage of fatty acids. Moreover, thiacremonone enhanced the mRNA level of carnitine palmitoyltransferase (CPT-1). The modulating effect of thiacremonone on expressions of genes involved in lipolysis was partially abrogated by treatment with compound C, an AMPK inhibitor. Taken together, these results indicated that thiacremonone-induced AMPK activation, inhibition of ACC-1 expression and concomitant recovery of CPT-1 expression resulted in the suppression of intracellular lipid droplet levels, suggesting that thiacremonone may induce reduction of lipid synthesis and increases in fatty acid oxidation partially mediated via AMPK activation. Thiacremonone may be a promising compound for the treatment of obesity.
大蒜提取物具有抗癌和抗炎作用。然而,大蒜衍生化合物的抗脂肪生成作用尚不清楚。在这项研究中,我们使用 3T3-L1 细胞研究了从大蒜中分离出的硫化合物硫代克劳酮对脂肪细胞分化的影响。我们发现,硫代克劳酮通过下调脂肪生成相关转录因子和脂肪生成标志物,显著抑制 3T3-L1 分化。这种抑制作用主要发生在 3T3-L1 细胞分化的早期阶段。硫代克劳酮在 3T3-L1 细胞中没有细胞毒性作用,用硫代克劳酮处理分化中的 3T3-L1 细胞会导致 AMPK 激活,从而减弱乙酰辅酶 A 羧化酶-1(ACC-1)的表达,ACC-1 是脂肪酸合成和利用的必需酶。此外,硫代克劳酮还能提高肉毒碱棕榈酰转移酶(CPT-1)的 mRNA 水平。用 AMPK 抑制剂化合物 C 处理部分消除了硫代克劳酮对脂解相关基因表达的调节作用。综上所述,这些结果表明,硫代克劳酮诱导的 AMPK 激活、ACC-1 表达抑制以及 CPT-1 表达的恢复导致细胞内脂滴水平降低,表明硫代克劳酮可能通过诱导部分 AMPK 激活来抑制脂质合成并增加脂肪酸氧化。硫代克劳酮可能是治疗肥胖的一种有前途的化合物。