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Treatment with Exercise and Genistein Improves Fracture Resistance in Mice Fed High‐Fat, High‐Sugar Diet

Diets high in fat and sugar (HFSD) adversely affect bone mineralization during growth and are implicated in osteoporosis in obese adults. In this study, we assessed fracture risk in mice fed a standard diet and mice fed HFSD. We evaluated fracture risk using three‐point bending tests and comparisons of cross‐sectional geometric properties of the femur. We also investigated the effects of low‐intensity exercise and dietary genistein, an isoflavone, on fracture risk in HFSD‐fed mice. We tested the hypothesis using 50 male and 50 female C57BL/6 mice aged six weeks, which we divided into five treatment groups: lean control, HFSD control, HFSD + exercise, HFSD + genistein, and HFSD + exercise + genistein. Lean control mice were fed standard rodent chow. HFSD consisted of chow with 60% fat content and drinking water with 42 g/L sugar (55% sucrose, 45% fructose). Exercise training consisted of treadmill running for 30 min/day, 5 days/week. Genistein was given at a dose of 600 mg/kg diet. Comparisons of body mass and blood plasma revealed mice fed HFSD were obese and hyperglycemic by the end of the 12‐week treatment period. Statistical analysis of the data showed no differences in cross‐sectional geometric properties in comparisons of lean and HSFD‐fed mice (P > 0.05). However, mice fed HFSD and treated with exercise and genistein had significantly increased maximum second moments of area relative to HFSD controls (P < 0.05). Femurs of these mice also exhibited greater ultimate force during three‐point bending tests (i.e. maximum force recorded at the time of fracture) than HFSD controls (P < 0.05). Femurs of HFSD‐fed mice treated with exercise and genistein also demonstrated reduced corrected total bone fluorescence (CTBF) relative to HFSD controls (P < 0.05). CTBF quantifies advanced glycation end products (AGEs) in bone matrix. It is an indicator of fracture risk related to increased bone brittleness and reflects a reduced capacity to deform under loading. Our findings show treatment with low intensity exercise and dietary genistein increased fracture resistance in mice fed HFSD. These results suggest exercise and genistein benefit bone health in individuals with HFSD‐induced obesity.