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首页> 外文期刊>The Journal of Nutritional Biochemistry >Thiacremonone, a sulfur compound isolated from garlic, attenuates lipid accumulation partially mediated via AMPK activation in 3T3-L1 adipocytes.
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Thiacremonone, a sulfur compound isolated from garlic, attenuates lipid accumulation partially mediated via AMPK activation in 3T3-L1 adipocytes.

机译:噻甲烯酮是一种从大蒜中分离出来的硫化合物,可减轻3T3-L1脂肪细胞中通过AMPK激活部分介导的脂质积累。

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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
机译:大蒜提取物发挥抗癌和抗炎作用。但是,大蒜衍生化合物的抗脂肪形成作用仍不清楚。在这项研究中,我们研究了从3T3-L1细胞中分离出的一种从大蒜中分离出来的硫化合物噻甲烯酮对脂肪细胞分化的影响。我们发现,噻甲烯酮可通过下调与脂肪形成相关的转录因子和脂肪形成标记来显着抑制3T3-L1分化。抑制作用主要发生在3T3-L1细胞分化的早期。噻克甲酮对3T3-L1细胞没有细胞毒性作用,用噻克甲酮处理分化的3T3-L1细胞导致AMPK活化,导致乙酰辅酶A羧化酶1(ACC-1)的表达减弱。脂肪酸的合成与使用。此外,噻甲烯酮可增强肉碱棕榈酰转移酶(CPT-1)的mRNA水平。通过用AMPK抑制剂化合物C处理,可以部分废除噻甲酮对脂解相关基因表达的调节作用。两者合计,这些结果表明,噻甲烯酮诱导的AMPK激活,ACC-1表达的抑制和CPT-1表达的同时恢复导致细胞内脂质滴水平的抑制,表明噻甲烯酮可能诱导脂质合成的减少和脂肪的增加。酸氧化部分通过AMPK激活介导。噻甲酮可能是治疗肥胖的有前途的化合物

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