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Updated: Sep 28, 2026

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
Published on: May 24, 2018
Effects of high-fat diet-induced obesity on circulating bone turnover markers in mice: a meta-analysis
Jie Ma1, Binglin Chen2, Bo Gao1
1Institute of Orthopedic Surgery, Xijing Hospital, Air force Medical University, Xi'an, Shaanxi, China.
Objective:
To investigate the level of bone turnover markers in the serum of mice induced into obesity by a high-fat diet, comparing them with non-obese counterparts.
Data Sources:
PubMed, Cochrane Library, Embase, EBSCO, and Web of Science were searched from database inception to July 22, 2026.
Methods:
Two researchers screened literature based on inclusion and exclusion criteria, extracting valid data for quality evaluation. meta-analysis was conducted using Review Manager 5.4 software, focusing on primary outcomes related to blood biochemical markers associated with bone metabolism, such as TRAP, CTX-1, and OCN levels.
Results:
Seven studies were included in the systematic review, of which five reported sufficiently comparable data for inclusion in the meta-analysis. Five articles, encompassing data from 256 mice, met the inclusion criteria. Compared to the non-obese group, the serum of obese mice exhibited a significant increase in TRAP levels (MD=1.68 U/L, 95% CI=1.08-2.27, P<0.00001) as well as CTX-1 levels (MD=9.87 ng/mL, 95% CI=5.53-14.22, P<0.00001), with no statistically significant difference in OCN levels (SMD=0.26, 95% CI=-0.78-1.30, P=0.63).
Conclusion:
Current evidence from a limited number of animal studies suggests that high-fat diet-induced obesity may be associated with increased circulating levels of selected bone resorption markers, including TRAP and CTX-I, in mice. No statistically significant difference was observed for OCN. Given the small number of studies, methodological limitations, substantial heterogeneity in the OCN analysis, and the absence of quantitative structural skeletal outcomes, these findings should be considered preliminary.