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首页> 外文期刊>RSC Advances >Divergent outcomes of gut microbiota alteration upon use of spectrum antibiotics in high sugar diet-induced diabetes in rats
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Divergent outcomes of gut microbiota alteration upon use of spectrum antibiotics in high sugar diet-induced diabetes in rats

机译：在大鼠高糖饮食诱导的糖尿病中使用光谱抗生素时，肠道微生物群改变的发散结果

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Background: A sugar rich diet induces inflammation and insulin resistance (IR) mainly through gut microbiota alteration. Gut dysbiosis increases lipopolysaccharide (LPS) and reduces propionate and butyrate levels to impair the insulin signalling cascades by different molecular pathways, which progresses into IR. The present study was designed to investigate the effect of spectrum specific antibiotics on the modulation of gut microbiota and its signalling pathways to prevent diet-induced diabetes. Methods: Healthy male Wistar rats were divided into a non-diabetic group with a control diet (CD), a diabetic group with a high sucrose diet (HSD) and two antibiotic fed groups (linezolid and cefdinir; administered by oral gavage) along HSD. Physiological, biochemical, inflammatory and microbiome parameters were examined. Results: Cefdinir administration in HSD rats reduced fasting glucose, serum triglyceride, and cholesterol levels compared to HSD alone. In addition, cefdinir reduced serum LPS by decreasing the population of Gram-negative phyla, that is, Bacteroidetes and Proteobacteria in the fecal content. Furthermore, cefdinir treatment decreased hepatic/ileal/colonic Tlr4, Nlr1, and Nf-kappa B at the mRNA level. Moreover, cefdinir-treated rats had shown increased fecal butyrate and propionate and reduced acetate levels compared to HSD alone. Cefdinir treatment also induced ileal/colonic Gpr43 and Glut4 at the mRNA level after 12 weeks of administration. Conclusions: Taken together, these data suggest that administration of a Gram-negative spectrum antibiotic, that is, cefdinir, has modulated the gut microbiota, and reduced serum LPS and triglycerides, which prevented the progression of IR and inflammation in HSD rats.
机译：背景：富含糖饮食诱导的炎症和胰岛素抵抗（IR）主要通过肠道菌群的改变。肠道生态失调的增加脂多糖（​​LPS），并降低丙酸和丁酸水平损害胰岛素信号通过不同的分子途径级联，其进展到IR。本研究旨在探讨的频谱特定抗生素对肠道微生物及其信号转导通路，防止饮食诱导的糖尿病的调节作用。方法：健康雄性Wistar大鼠分为非糖尿病组与对照饮食（CD），具有高蔗糖饮食（HSD）和两个抗生素馈团的糖尿病组;沿着HSD（利奈唑胺和头孢地尼通过口服管饲法给药） 。生理，检查生化，炎症和微生物参数。结果：头孢地尼政府在HSD大鼠降低空腹血糖，血清甘油三酯，并比单独HSD胆固醇水平。此外，头孢地尼减少的血清通过减小革兰氏阴性门类，即，拟杆菌和变形菌在粪便内容的人口LPS。此外，头孢地尼治疗在mRNA水平降低的肝/回肠/结肠TLR4，Nlr1，和NF-κB的。此外，头孢地尼治疗的大鼠表明增加粪便丁酸和丙和单独相比HSD减少乙酸酯水平。头孢地尼的治疗也可诱导回肠/结肠GPR43化和Glut4在12周给药后的mRNA水平。结论：总之，这些数据表明革兰氏阴性广谱抗生素，即，头孢地尼的给药，已调制的肠道菌群和减少的血清LPS和甘油三酯，其防止红外在HSD大鼠的进展和炎症。

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