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Bacterial cell wall components regulate adipokine secretion from visceral adipocytes

机译:细菌细胞壁成分调节内脏脂肪细胞分泌的脂肪因子

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摘要

Recent studies suggest a relationship between intestinal microbiota and metabolic syndromes; however, the underlying mechanism remains unclear. To clarify this issue, we assessed the effects of bacterial cell wall components on adiponectin, leptin and resistin secretion from rat visceral adipocytes in vitro. We also measured the relative population of Firmicutes and Bacteroidetes in fecal microbiota and the amount of fecal mucin as an intestinal barrier function, when mice were fed a high-fat diet. In the present study, we demonstrated that bacterial cell wall components affect the secretion of adipokines, depending on the presence of antigens from gram-positive or gram-negative bacteria. Lipopolysaccharide markedly inhibited adiponectin, leptin, and resistin secretion, whereas peptidoglycan increased adiponectin secretion and decreased resistin secretion in vitro. In vivo experiments showed that the high-fat diet increased the population of Firmicutes and decreased that of Bacteroidetes. In contrast, the high-fat diet downregulated the stool output and fecal mucin content. These results demonstrate that bacterial cell wall components affect the onset of metabolic syndromes by mediating the secretion of adipokines from visceral adipose tissue. Furthermore, we believe that metabolic endotoxemia is not due to the increasing dominance of gram-negative bacteria, Bacteroidetes, but due to the depression of intestinal barrier function.
机译:最近的研究表明肠道菌群与代谢综合征之间存在相关性。但是,其潜在机制仍不清楚。为了澄清这个问题,我们评估了细菌细胞壁成分对大鼠内脏脂肪细胞中脂联素,瘦素和抵抗素分泌的影响。当小鼠接受高脂饮食时,我们还测量了粪便微生物群中Firmicutes和Bacteroidetes的相对种群,以及作为肠道屏障功能的粪便粘蛋白的量。在本研究中,我们证明了细菌细胞壁成分会影响脂肪因子的分泌,具体取决于革兰氏阳性或革兰氏阴性细菌的抗原存在。脂多糖显着抑制脂联素,瘦素和抵抗素的分泌,而肽聚糖在体外增加脂联素的分泌并降低抵抗素的分泌。体内实验表明,高脂饮食增加了Firmicutes的种群,减少了拟杆菌的种群。相反,高脂饮食下调了粪便产量和粪便粘蛋白含量。这些结果表明,细菌细胞壁成分通过介导内脏脂肪组织分泌脂肪因子而影响代谢综合征的发作。此外,我们认为代谢性内毒素血症不是由于革兰氏阴性细菌(拟杆菌)的优势地位增加,而是由于肠屏障功能的降低。

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