Diet is one of the risk factors for osteoporosis in addition to heredity, age, oestrogen deficiency, and calcium and phosphorus metabolism. Whether FO has a protective effect on HFD-induced bone damage has not been clarified, and the specific mechanism of bone protection is unclear. Therefore, this study aimed to evaluate whether totally replacing soybean oil and partly replacing lard with FO in HFD can improve high-fat-induced bone damage in vivo. We treated rat primary OBs with ALA in vitro to observe the effect of ALA on osteoblastic function, osteogenic-related gene and protein expression and tried to explore the mechanism of ALA on bone protection. The major finding of this study was that FO alleviated bone loss in HFD rats. Meanwhile, ALA can promote primary osteoblastic function through increasing β-catenin/RUNX2/osterix genes and proteins expression and restoring PA induced ALP activity decreases. The current study also focused on male rats, and trabecular bone loss was observed in HFD induced male SD rats. The bone loss induced by HFD was attenuated by treatment with FO, as shown by micro-CT, three-point bending test and bone histology analysis. The results showed that ALA dramatically promoted β-catenin gene and protein expression in OBs, which suggested that ALA may promote osteogenic differentiation through the Wnt pathway. In the present study, the main finding was that FO alleviated bone loss in HFD rats, probably by promoting osteoblastic β-catenin/RUNX2/osterix gene and protein expression and restoring PA-induced ALP activity decreases. These findings indicated that FO might be a potential therapeutic agent for HFD-induced bone loss, most likely by promoting osteogenesis.
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