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首页> 外文期刊>Journal of Hepatology: The Journal of the European Association for the Study of the Liver >Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.
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Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.

机译:益生菌可通过增加肝脏NKT细胞来改善高脂饮食诱导的肝脂肪变性和胰岛素抵抗。

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摘要

BACKGROUND/AIMS: Dietary factors and intestinal bacteria play an important role in the rapidly increasing incidence of obesity and its associated conditions, such as steatosis and insulin resistance. In the current study, we evaluated the effect of probiotics, and their mechanisms on diet-induced obesity, steatosis and insulin resistance. METHODS: Wild-type male C57BL6 mice were fed either normal or high fat diets. Some mice received VSL#3 probiotics. Animal weight, hepatic steatosis, insulin resistance, and their relationship to hepatic Natural Killer T cells (NKT) cell number and inflammatory signaling were evaluated. RESULTS: High fat diet induced a depletion of hepatic NKT cells thus leading to insulin resistance and steatosis. Oral probiotic treatment significantly improved the high fat diet-induced hepatic NKT cell depletion, insulin resistance and hepatic steatosis. This effect was NKT cell dependant, resulted from the attenuation of the tumor necrosis factor-alpha and IkappaB kinase inflammatory signaling, and led to an improved sensitivity in insulin signaling. CONCLUSIONS: Probiotics improve high fat diet-induced steatosis and insulin resistance. These effects of probiotics are likely due to increased hepatic NKT cell numbers and reduced inflammatory signaling.
机译:背景/目的:饮食因素和肠道细菌在肥胖及其相关状况(例如脂肪变性和胰岛素抵抗)的发病率迅速增加中起着重要作用。在当前的研究中,我们评估了益生菌的作用及其对饮食诱导的肥胖,脂肪变性和胰岛素抵抗的作用机理。方法:给野生型C57BL6雄性小鼠喂食正常或高脂饮食。一些小鼠接受了VSL#3益生菌。评估了动物的体重,肝脂肪变性,胰岛素抵抗及其与肝天然杀伤性T细胞(NKT)细胞数量和炎症信号的关系。结果:高脂饮食诱导肝NKT细胞耗竭,从而导致胰岛素抵抗和脂肪变性。口服益生菌治疗可显着改善高脂饮食诱导的肝NKT细胞耗竭,胰岛素抵抗和肝脂肪变性。该作用是NKT细胞依赖性的,这是由于肿瘤坏死因子-α和IkappaB激酶炎性信号传导的减弱所致,并导致胰岛素信号传导的敏感性提高。结论:益生菌可改善高脂饮食引起的脂肪变性和胰岛素抵抗。益生菌的这些作用可能是由于肝脏NKT细胞数量增加和炎症信号减少所致。

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