Objective To study the effect of vitamin D treatment on bone metastasis of prostate cancer mice induced by octanoic acid and high⁃fat diet. Methods The bone metastasis model of prostate cancer mice was established，and the mice were divided into normal feeding Control group，High fat group fed with high fat diet， Bitter group fed with caprylic acid and Vitamin D group fed with caprylic acid and high fat diet. After the study， the contents of total cholesterol，triglyceride，low⁃density lipoprotein，calcium and 25⁃hydroxyvitamin D（25⁃OH⁃D） in peripheral blood of mice in the three groups were detected，and the degree of bone metastasis and the expression of E⁃cadherin and p38 protein in tumor tissues of mice in each group were detected. Transwell mice were used in vitro to study the effect of vitamin D on the invasion and migration ability of RM⁃1 cells affected by caprylic acid. Results Compared with the control group，the contents of total cholesterol，triglyceride，low density lipoprotein and calcium in the blood of mice in the High fat group and Bitter group，as well as the contents of SUVmin，SUVmax and SUVmean in the 18F⁃NaF PET⁃CT test results were significantly increased（P < 0.05）；And Bitter group was significantly higher than High fat group（P < 0.05），while Vitamin D group was significantly lower than Bitter group（P < 0.05）. In vitro，octanoic acid treatment significantly increased the invasion and migration ability of RM⁃1 cells，but vitamin D could inhibit the invasion and migration ability of RM⁃1 cells promoted by octanoic acid. In vivo，caprylic acid can significantly increase the expression of E⁃cadherin and p⁃p38/p38 protein in tumor tissue of mice with bone metasta⁃ sis of prostate cancer from high⁃fat diet，but vitamin D can significantly reduce the increased E⁃cadherin and p⁃p38/ p38 protein table of caprylic acid. Conclusion Vitamin D treatment inhibited bone metastasis of prostate cancer mice promoted by octanoic acid and high⁃fat diet，and its mechanism may be related to the increase of serum 25⁃OH⁃D content and the inhibition of E⁃cadherin，p⁃p38/p38 protein expression in cancer cells.