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首页> 外文期刊>The Journal of Nutritional Biochemistry >Involvement of SIRT1-AMPK signaling in the protective action of indole-3-carbinol against hepatic steatosis in mice fed a high-fat diet.
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Involvement of SIRT1-AMPK signaling in the protective action of indole-3-carbinol against hepatic steatosis in mice fed a high-fat diet.

机译：SIRT1-AMPK信号传导参与高脂饮食小鼠中吲哚-3-甲醇对肝脂肪变性的保护作用。

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This study addressed the effect of indole-3-carbinol (I3C) supplementation on hepatic steatosis in mice fed a high-fat diet (HFD) and clarified the underlying mechanism. Male C57BL/6N mice were divided into three groups: those who received a normal diet, those fed with HFD and those fed with 0.1% I3C-supplemented diet (I3CD). In the present study, an HFD supplemented with 0.1% I3C significantly decreased body and liver weight as well as plasma and hepatic lipid levels. The activation of the silent mating type information regulation 2 homolog 1 (SIRT1)-AMP-activated protein kinase (AMPK) signaling system by I3C correlated with decreased mRNA levels of sterol regulatory element-binding protein-1c-regulated lipogenic enzymes. In addition, I3C significantly reversed HFD-induced up-regulation of ER stress-mediated signaling molecules in the liver, which may have contributed to the protective effects of I3C against hepatic steatosis. Furthermore, HFD-induced up-regulations of inflammatory genes such as tumor necrosis factor alpha and interleukin 6 were significantly reversed by dietary I3C supplementation. Our study suggests that the protective action of I3C against hepatic steatosis is mediated, at least in part, through the up-regulation of a SIRT1-AMPK signaling system in the livers of HFD-fed mice. Further investigations revealed that alleviation of the ER stress response represented a critical mechanism underlying the beneficial effects of I3C on hepatic steatosis
机译：这项研究解决了补充吲哚-3-甲醇（I3C）对高脂饮食（HFD）喂养的小鼠肝脂肪变性的影响，并阐明了其潜在机制。将雄性C57BL / 6N小鼠分为三组：正常饮食，HFD喂养和0.1％I3C补充饮食（I3CD）喂养的小鼠。在本研究中，补充有0.1％I3C的HFD可以显着降低体重和肝脏重量以及血浆和肝脂质水平。 I3C对沉默交配型信息调节2同源物1（SIRT1）-AMP激活的蛋白激酶（AMPK）信号系统的激活与固醇调节元件结合蛋白1c调节的脂肪酶的mRNA水平降低有关。另外，I3C显着逆转了HFD诱导的肝脏中ER应激介导的信号分子的上调，这可能有助于I3C对肝脂肪变性的保护作用。此外，通过补充饮食中的I3C可以显着逆转HFD诱导的炎症基因（如肿瘤坏死因子α和白介素6）的上调。我们的研究表明I3C对肝脂肪变性的保护作用至少部分是通过HFD喂养的小鼠肝脏中SIRT1-AMPK信号系统的上调来介导的。进一步的研究表明，减轻ER应激反应是I3C对肝脂肪变性有益作用的关键机制。

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