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在 C57BL/6 小鼠中操纵肠道微生物群会改变葡萄糖耐量,而不影响体重发育和肠道黏膜免疫。

Manipulation of the gut microbiota in C57BL/6 mice changes glucose tolerance without affecting weight development and gut mucosal immunity.

机构信息

Department of Veterinary Disease Biology, Faculty of Life Sciences, University of Copenhagen, Grønnegårdsvej 18, DK-1870 Frederiksberg, Denmark.

出版信息

Res Vet Sci. 2012 Jun;92(3):501-8. doi: 10.1016/j.rvsc.2011.04.005. Epub 2011 May 2.

DOI:10.1016/j.rvsc.2011.04.005
PMID:21543097
Abstract

Inflammatory diseases such as type 2 diabetes (T2D) in humans and mice are under the influence of the composition of the gut microbiota (GM). It was previously demonstrated that treating Lep(ob) mice with antibiotics improved glucose tolerance. However, wild type C57BL/6J mice may also exhibit plasma glucose intolerance reminiscent of human T2D. We hypothesized that antibiotic treatment in C57BL/6 mice would have an impact on glucose tolerance without affecting weight and gut immunology. When compared to mice treated with erythromycin or the controls, treatment for five weeks with ampicillin improved glucose tolerance without significantly affecting the weight or the number of gut mucosal regulatory T cells, tolerogenic dendritic cells or T helper cells type 1. 16S rRNA gene based denaturing gradient gel electrophoresis profiles clearly clustered according to treatment and showed that antibiotic treatment reduced GM diversity. It is concluded that antibiotic treatment changes glucose metabolism as well as the composition of the GM in C57BL/6 mice, and that this does not seem to be correlated to weight development in the mice.

摘要

在人类和小鼠中,炎症性疾病(如 2 型糖尿病(T2D))受到肠道微生物群(GM)组成的影响。先前的研究表明,用抗生素治疗 Lep(ob)小鼠可以改善葡萄糖耐量。然而,野生型 C57BL/6J 小鼠也可能表现出类似于人类 T2D 的血浆葡萄糖不耐受。我们假设,在 C57BL/6 小鼠中使用抗生素治疗会对葡萄糖耐量产生影响,而不会影响体重和肠道免疫。与用红霉素或对照组治疗的小鼠相比,用氨苄青霉素治疗五周可改善葡萄糖耐量,而不会显著影响体重或肠道粘膜调节性 T 细胞、耐受性树突状细胞或 T 辅助细胞 1 的数量。基于 16S rRNA 基因的变性梯度凝胶电泳图谱根据治疗方法明显聚类,并表明抗生素治疗可降低 GM 多样性。研究结论认为,抗生素治疗可改变 C57BL/6 小鼠的葡萄糖代谢和 GM 组成,而这似乎与小鼠的体重增长无关。

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