Division of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin, China.
Sci Rep. 2019 Mar 13;9(1):4381. doi: 10.1038/s41598-019-40978-9.
Gut microbiota plays a pivotal role in various aspects of host physiology, including metabolism, gastrointestinal (GI) motility and hormonal secretion. In the present study, we investigated the effect of antibiotic-associated dysbiosis on metabolism and GI motility in relation to colonic expression of glucagon-like peptide-1 (GLP-1) and G protein coupled receptor (GPR)43. Specific pathogen-free (SPF) mice (ICR, 6 weeks old, female) were orally administered vancomycin (0.2 mg/ml) in drinking water for 7 days. In another experiment, germ-free (GF) mice (ICR, 6 weeks old, female) were subjected to oral fecal transplantation (FT) using a fecal bacterial suspension prepared from SPF mice that had received vancomycin treatment (FT-V) or one from untreated control SPF mice (FT-C). The gastrointestinal transit time (GITT) was measured by administration of carmine red (6% w/v) solution. The expression of GLP-1 and GPR43 was examined by immunohistochemistry and realtime RT-PCR, and the plasma GLP-1 level was measured by ELISA. In vancomycin-treated SPF mice, the diversity of the gut microbiota was significantly reduced and the abundance of Lactobacillus was markedly increased. Significant increases in body weight, cecum weight, plasma GLP-1 level and colonic GLP-1/GPR43 expression were also noted relative to the controls. These alterations were reproducible in GF mice with FT-V. Moreover, FT-V GF mice showed a significantly increased food intake and a significantly prolonged GITT in comparison with FT-C GF mice. Vancomycin-induced dysbiosis promotes body weight gain and prolongs GITT, accompanied by an increase of colonic GLP-1/GPR43 expression.
肠道微生物群在宿主生理学的各个方面发挥着关键作用，包括代谢、胃肠道 (GI) 运动和激素分泌。在本研究中，我们研究了抗生素相关的菌群失调对代谢和 GI 运动的影响，以及与结肠中胰高血糖素样肽-1 (GLP-1) 和 G 蛋白偶联受体 (GPR)43 的表达有关。使用含 0.2mg/ml 万古霉素的饮用水对无特定病原体 (SPF) 小鼠（ICR，6 周龄，雌性）进行口饲，持续 7 天。在另一个实验中，使用来自接受万古霉素处理的 SPF 小鼠（FT-V）或未处理的对照 SPF 小鼠（FT-C）的粪便细菌混悬液对无菌 (GF) 小鼠（ICR，6 周龄，雌性）进行口服粪便移植 (FT)。通过给予胭脂红（6%w/v）溶液来测量胃肠道转运时间 (GITT)。通过免疫组织化学和实时 RT-PCR 检查 GLP-1 和 GPR43 的表达，并通过 ELISA 测量血浆 GLP-1 水平。在万古霉素处理的 SPF 小鼠中，肠道微生物群的多样性显著降低，而乳酸杆菌的丰度显著增加。与对照组相比，体重、盲肠重量、血浆 GLP-1 水平和结肠 GLP-1/GPR43 表达也显著增加。在接受 FT-V 的 GF 小鼠中也重现了这些改变。此外，与接受 FT-C 的 GF 小鼠相比，FT-V GF 小鼠的食物摄入量显著增加，GITT 显著延长。万古霉素诱导的菌群失调促进体重增加，并延长 GITT，同时结肠 GLP-1/GPR43 表达增加。
