The hypothesis of the present study was that physical activity improves diet-induced obesity in young adult mice. Four-week-old male C57BL/6 mice (n=15/group) were fed the AIN93G diet or a 45% high-fat diet (% kJ) with or without access to in-cage activity wheels for 14 weeks. The high-fat diet increased percentage fat body mass compared to the AIN93G diet (P=.042); running reduced percentage fat body mass (P<.0001) and increased percentage lean body mass (P<.0001) in mice fed either diet. Compared with the AIN93G diet, the high-fat diet increased plasma concentrations of insulin (P<.05) and leptin (P<.05) in sedentary mice and inflammatory cytokines monocyte chemotactic protein-1 (MCP-1) (P<.05) and plasminogen activator inhibitor-1 (P<.05) in both sedentary and running mice. The high-fat diet did not affect angiogenic factors vascular endothelial growth factor and platelet-derived growth factor-BB. Running reduced plasma insulin (P<.05) and MCP-1 (P<.05) and increased platelet-derived growth factor-BB (P<.05) in mice fed the high-fat diet. Running reduced leptin (P<.05) and increased plasma vascular endothelial growth factor (P<.0001) regardless of diet fed. In summary, consumption of the high-fat diet increased adiposity in young adult mice; running reduced adiposity, normalized plasma insulin and leptin, and reduced MCP-1 despite continued consumption of the high-fat diet. These results suggest that voluntary running may reduce diet-induced obesity and proinflammation and that young mice may be a useful model of their human age equivalents in studying moderate physical exercise and obesity and obesity-related diseases.
