title: Different contribution of muscle and liver lipid metabolism to endurance capacity and obesity susceptibility of mice.
abstract: We investigated strain differences in whole body energy metabolism, peripheral lipid metabolism, and energy metabolism-related gene expression and protein levels in BALB/c, C57BL/6J, and A/J mice to evaluate the relationship between endurance capacity, susceptibility to diet-induced obesity, and differences in lipid metabolism in muscle and liver. A high-fat diet significantly increased body weight and fat weight in C57BL/6J mice, but not in BALB/c and A/J mice. The endurance capacity of BALB/c mice was 52% greater than that of C57BL/6J mice and 217% greater than that of A/J mice. The respiratory exchange ratio was lowest in BALB/c mice, higher in C57BL/6J mice, and highest in A/J mice, which inversely correlated with the endurance capacity and fatty acid beta-oxidation activity in the muscle. Plasma lactate levels measured immediately after exercise were lowest in BALB/c mice and highest in A/J mice, although there was no difference under resting conditions, suggesting that carbohydrate breakdown is suppressed by enhanced fat utilization during exercise in BALB/c mice. On the other hand, the body weight increase induced by high-fat feeding was related to a reduced whole body energy expenditure, higher respiratory quotient, and lower fatty acid beta-oxidation activity in the liver. In addition, beta-oxidation activity in the muscle and liver roughly paralleled the mRNA and protein levels of lipid metabolism-related molecules, such as peroxisome proliferator-activated receptor and medium-chain acyl-CoA dehydrogenase, in each tissue. These findings indicate that genetically determined basal muscle and liver lipid metabolism and responsiveness to exercise influence physical performance and obesity susceptibility.
authors.affiliation: Biological Science Laboratories, Kao Corporation, Ichikai-machi, Haga-gun, Tochigi, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Haramizu
authors.forename: Azumi
authors.initials: A
authors.lastname: Nagasawa
authors.forename: Noriyasu
authors.initials: N
authors.lastname: Ota
authors.forename: Tadashi
authors.initials: T
authors.lastname: Hase
authors.forename: Ichiro
authors.initials: I
authors.lastname: Tokimitsu
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Murase
mesh_terms: D042964:Acyl-CoA Dehydrogenase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects / Q000235:genetics*; D005227:Fatty Acids / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D009765:Obesity / Q000209:etiology / Q000235:genetics*; D010084:Oxidation-Reduction / Q000187:drug effects; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism; D010807:Physical Endurance / Q000187:drug effects / Q000235:genetics*; D013045:Species Specificity; D015430:Weight Gain / Q000187:drug effects / Q000235:genetics
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids; D047493:PPAR alpha; D042964:Acyl-CoA Dehydrogenase