High-fat diet (HFD)-induced obese-insulin resistance negatively affects bone via gut microbiota dysbiosis-triggered systemic inflammation. The biotic treatment can improve metabolic status in HFD-fed rats. However, the microarchitectural analysis by bone histomorphometry of the tibia have not been determined. Forty-eight male Wistar rats were fed with normal diet or HFD for 24 weeks. At week13, rats were received either a vehicle, Lactobacillus paracasei HII01, xylooligosaccharides, or synbiotics. Blood analyses and tibial histomorphometry were performed. We found that L. paracasei HII01, xylooligosaccharides, and synbiotics improved obese-insulin resistance and systemic inflammation in HFD-fed rats. These biotics equally increased bone volume fraction and trabecular thickness, reduced osteoclast surface and active erosion surface, increased the double labeled surface, mineralizing surface, mineral apposition rate and bone formation rate of HFD-fed rats. In conclusion, these biotic therapies exerted an enhancement of bone microarchitecture in HFD-fed rats possibly by mitigating osteoclast-mediated bone resorption and promoting osteoblast-induced bone formation.

高脂饮食（HFD）引起的肥胖胰岛素抵抗会通过肠道菌群失调触发的全身性炎症对骨骼产生负面影响。生物治疗可以改善HFD喂养的大鼠的代谢状况。然而，尚未确定通过胫骨的骨组织形态学进行的微结构分析。48只雄性Wistar大鼠用正常饮食或HFD喂养24周。在第13周，大鼠接受媒介物，副干酪乳杆菌HII01，木寡糖或合生元。进行血液分析和胫骨组织形态测量。我们发现副干酪乳杆菌HII01，低聚木糖和合生素改善了由HFD喂养的大鼠的肥胖胰岛素抵抗和全身性炎症。这些生物同样增加了HFD喂养的大鼠的骨体积分数和小梁厚度，减少了破骨细胞表面和活跃的侵蚀表面，增加了双标记表面，矿化表面，矿物质沉积率和骨形成率。总之，这些生物疗法可能通过减轻破骨细胞介导的骨吸收并促进成骨细胞诱导的骨形成而增强了由HFD喂养的大鼠的骨微结构。