益生菌通过增加肝脏自然杀伤T细胞来改善高脂饮食诱导的肝脂肪变性和胰岛素抵抗。
Probiotics improve high fat diet-induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells.
作者信息
Ma Xiong, Hua Jing, Li Zhiping
机构信息
Department of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
出版信息
J Hepatol. 2008 Nov;49(5):821-30. doi: 10.1016/j.jhep.2008.05.025. Epub 2008 Jun 30.
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.
背景/目的：饮食因素和肠道细菌在肥胖及其相关病症（如脂肪变性和胰岛素抵抗）发病率迅速上升中起重要作用。在本研究中，我们评估了益生菌对饮食诱导的肥胖、脂肪变性和胰岛素抵抗的影响及其作用机制。
方法
将野生型雄性C57BL6小鼠分为正常饮食组和高脂饮食组。部分小鼠给予VSL#3益生菌。评估动物体重、肝脏脂肪变性、胰岛素抵抗，以及它们与肝脏自然杀伤T细胞（NKT）数量和炎症信号的关系。
结果
高脂饮食导致肝脏NKT细胞减少，从而引起胰岛素抵抗和脂肪变性。口服益生菌治疗显著改善了高脂饮食诱导的肝脏NKT细胞减少、胰岛素抵抗和肝脏脂肪变性。这种作用依赖于NKT细胞，是由肿瘤坏死因子-α和IκB激酶炎症信号减弱所致，并导致胰岛素信号敏感性提高。
结论
益生菌可改善高脂饮食诱导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。
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