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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #277492
Title: Long-term voluntary running improves diet-induced adiposity in young adult mice

Author
item Yan, Lin
item Demars, Lana
item JOHNSON, LUANN - University Of North Dakota

Submitted to: Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/16/2012
Publication Date: 6/18/2012
Citation: Yan, L., Demars, L.C., Johnson, L.K. 2012. Long-term voluntary running improves diet-induced adiposity in young adult mice. Nutrition Research. 32:458-465.

Interpretive Summary: Overweight and obesity among children and adolescents continue to be a public health concern in the United States. Decreased physical activity and consumption of hypercaloric diets contribute to the prevalence of overweight and obesity. The authors investigated the effects of long-term voluntary running on diet-induced obesity in mice at their life phase equivalent to humans from adolescents to young adults. Four-week old mice (15 per group) were fed a normal control diet or a 45% high-fat diet (% kcal.) with or without access to in-cage activity wheels from sexual maturation for 14 weeks. The high-fat diet significantly increased fat body mass compared with the control diet; voluntary running significantly reduced fat body mass and increased lean body mass in the high-fat diet-fed mice. The high-fat diet significantly increased plasma concentrations of insulin and adipose-associated inflammatory cytokines leptin, monocyte chemotactic protein-1 (MCP-1) and plasminogen activator inhibitor-1 (PAI-1) compared with the control diet. Running significantly reduced plasma insulin, leptin and MCP-1, but not PAI-1, in the high-fat diet-fed mice compared with their respective sedentary controls. In summary, young adult mice responded to both the high-fat diet and non-motorized voluntary running with changes in body compositions and inflammatory biomarkers, indicating they may be useful to model their human equivalents adolescents and young adults in studying moderate physical activity and diet-induced obesity.

Technical Abstract: The present study investigated the effects of long-term voluntary running on diet-induced adiposity in male C57BL/6 mice. Four-week old mice (n = 15 per group) were fed the AIN93G diet or a 45% high-fat diet (% kcal.) with or without access to in-cage activity wheels for 14 weeks. The high-fat diet increased fat body mass compared with the AIN93G diet (P = 0.042), which accounted for increases in body weight gain (P = 0.035); voluntary running reduced fat body mass (P < 0.0001) and increased lean body mass (P < 0.0001) in mice fed either diet. The high-fat diet increased plasma concentrations of insulin (P < 0.05), leptin (P < 0.05) and inflammatory cytokines monocyte chemotactic protein-1 (MCP-1; P < 0.05) and plasminogen activator inhibitor-1 (PAI-1; P < 0.05) but not angiogenic factors vascular endothelial growth factor (VEGF) and platelet-derived growth factor-BB (PDGF-BB), compared with the AIN93G diet. Running reduced plasma insulin (P < 0.05), leptin (P < 0.05) and MCP-1 (P < 0.05), but not PAI-1, and increased plasma PDGF-BB in the high-fat diet-fed mice (P < 0.05) and VEGF in mice fed either diet (P < 0.0001) compared with their respective sedentary controls. In summary, consumption of the high-fat diet increased adiposity in young adult mice; long term voluntary running reduced adiposity, normalized plasma insulin and leptin and reduced MCP-1 despite continued consumption of the high-fat diet. The adiposity-associated angiogenesis by the high-fat diet may be through mechanisms not mediated by VEGF and PDGF-BB, and increases of VEGF and PDGF-BB by running may be a direct response of capillary growth in skeletal muscles to exercise.