Abstract：
Gut microbiota (GM) dysbiosis is closely related to several metabolic diseases such as hypertension, obesity, and Alzheimer\'s disease. However, little is known about the causal relationship between GM dysbiosis and osteoporosis. In our work, 32 3-month-old female SD rats were randomly divided into two groups: the fecal microbiota transplantation (FMT) group and the control group. The supernatant of feces from senile osteoporotic rats was transplanted to the FMT group and the same amount of sterile saline was given to the control rats. After 12 and 24 weeks, all rats were sacrificed, and the serum, bone, fecal feces, and intestine tissue were collected for the subsequent analysis. The osteocalcin (OC), CTX, and P1NP of the FMT group increased significantly at 12 and 24 weeks compared with the control group (P < 0.05). Furthermore, the BV, BV/TV, Tb.N, and Tb.Th decreased significantly in the FMT group (P < 0.05). The alpha diversity (ACE, Chao) of the FMT group was higher than the control at 24 weeks (P < 0.05). The beta diversity was close between the FMT rats and the donor rats. In addition, GM from donor rats changed the GM composition and function of the FMT rats, which was similar to that of the donor rats at 24 weeks. The impaired intestinal structure and the decreased expression of occludin, claudin, and ZO-1 were found in FMT rats. In conclusion, GM dysbiosis by transferring the feces from senile osteoporotic rats to young rats could induce osteoporosis. The changed GM and the impaired intestinal barrier contributed to the pathogenesis of osteoporosis.
摘要：
肠道微生物群(GM)菌群失调与高血压等几种代谢性疾病密切相关,肥胖，和老年痴呆症。然而,对转基因菌群失调和骨质疏松症之间的因果关系知之甚少。在我们的工作中,将32只3月龄雌性SD大鼠随机分为粪菌移植(FMT)组和对照组。将老年骨质疏松大鼠粪便上清液移植至FMT组，对照组大鼠给予等量无菌生理盐水。12周和24周后，所有的老鼠都被处死,还有血清,骨头,粪便粪便,收集肠组织用于后续分析。骨钙蛋白（OC），CTX,与对照组相比，FMT组的P1NP在12周和24周时明显升高（P<0.05）。此外，BV,BV/TV,TB。N,Tb。FMT组Th显著下降(P<0.05)。阿尔法多样性(ACE，24周时，FMT组的Chao）高于对照组（P<0.05）。β多样性在FMT年夜鼠和供体年夜鼠之间接近。此外,来自供体大鼠的GM改变了FMT大鼠的GM组成和功能，这与24周时的供体大鼠相似。肠道结构受损和occludin表达减少，Claudin,在FMT大鼠中发现了ZO-1。总之,通过将老年骨质疏松大鼠的粪便转移到年轻大鼠的GM菌群失调可以诱发骨质疏松症。改变的GM和受损的肠屏障是骨质疏松症的发病机制。
