Lactobacillus sakei OK67 ameliorates high-fat diet-induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression
Lactobacillus sakei OK67 ameliorates high-fat diet-induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression
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DOI：
10.1016/j.nutres.2015.12.001
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发表时间：
2016-04-01
影响因子：
4.5
通讯作者：
Kim, Dong-Hyun
中科院分区：
文献类型：
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作者：
Lim, Su-Min;Jeong, Jin-Ju;Kim, Dong-Hyun
高脂饮食（HFD）通过肠道微生物群、内毒素血症和肠道通透性增加的变化诱导肥胖和相关的血糖和炎症增加。为了抵消这一点，研究人员建议使用益生菌抑制促炎脂多糖（LPS）的产生。在这里，我们测试了从泡菜中分离的乳酸菌中选择的抑制肠道微生物群LPS产生的清酒乳杆菌OK 67是否在HFD喂养的小鼠中发挥抗低血糖或抗炎作用。将小鼠随机分为2组，并喂食HFD或低脂饮食4周。将这些组进一步细分; 1个亚组用L sakei OK 67处理并饲喂实验饲料4.5周，而另一个亚组仅饲喂实验饲料。Lsakei OK 67治疗降低了血液和结肠液中HFD升高的LPS水平，并显著降低了口服葡萄糖耐量试验中HFD升高的空腹血糖水平和曲线下面积。L sakei OK 67处理抑制HFD诱导的身体和附睾脂肪重量增加，抑制结肠中HFD诱导的肿瘤坏死因子a和白细胞介素-1 β表达和核因子-κ B活化，并显著增加结肠中HFD抑制的白细胞介素-10和紧密连接蛋白表达。口服L Sakei OK 67显著下调HFD诱导的脂肪组织中过氧化物酶体增殖物激活受体γ、脂肪酸合成酶和肿瘤坏死因子α的表达。此外，L sakei OK 67处理强烈抑制LPS刺激的腹腔巨噬细胞中的核因子-κ B活化。我们报告，L sakei OK 67通过减少炎症和增加小鼠结肠紧密连接蛋白的表达来改善HFD诱导的高血糖和肥胖。(C)2016 Elsevier Inc. All rights reserved.
A high-fat diet (HFD) induces obesity and the associated increases in blood glucose and inflammation through changes in gut microbiota, endotoxemia, and increased gut permeability. To counteract this, researchers have suggested that the use of probiotics that suppress production of proinflammatory lipopolysaccharide (LPS). Here, we tested whether Lactobacillus sakei OK67, which inhibits gut microbiota LPS production selected from among the lactic acid bacteria isolated from kimchi, exerted antihypoglycemic or anti-inflammatory effects in HFD-fed mice. Mice were randomly divided into 2 groups and fed an HFD or a low-fat diet for 4 weeks. These groups were further subdivided; 1 subgroup was treated with L sakei OK67 and fed the experimental diet for 4.5 weeks, whereas the other subgroup was fed the experimental diet alone. L sakei OK67 treatment lowered HFD-elevated LPS levels in blood and colonic fluid and significantly decreased HFD-elevated fasting blood glucose levels and the area under the curve in an oral glucose tolerance test. L sakei OK67 treatment inhibited HFD-induced body and epididymal fat weight gains, suppressed HFD-induced tumor necrosis factor a and interleukin-1 beta expression and nuclear factor-kappa B activation in the colon, and significantly increased HFD-suppressed interleukin-10 and tight junction protein expression in the colon. Oral administration of L sakei OK67 significantly downregulated HFD-induced expression of peroxisome proliferator-activated receptor gamma, fatty acid synthase, and tumor necrosis factor a in adipose tissue. In addition, L sakei OK67 treatment strongly inhibited nuclear factor-kappa B activation in LPS-stimulated peritoneal macrophages. We report that L sakei OK67 ameliorates HFD-induced hyperglycemia and obesity by reducing inflammation and increasing the expression of colon tight junction proteins in mice. (C) 2016 Elsevier Inc. All rights reserved.