title: Efficiency of energy retention in genetically obese animals and in dietary-induced thermogenesis.
abstract: Genetically obese rodents (ob/ob mice and fa/fa rats) and animals with dietary-induced thermogenesis represent two extremes in efficiency of energy retention: the former deposit dietary energy with high efficiency, whereas the later deposit dietary energy with low efficiency. These differences in efficiency of energy retention must, at the cellular level, be associated with changes in efficiency and/or rate of formation and/or utilization of ATP (and other high energy intermediates). Brown adipose tissue possesses a unique proton-conductance pathway that reduces the efficiency of ATP synthesis. It has been speculated that this pathway is suppressed in obese (ob/ob) mice and accelerated in rats with dietary-induced thermogenesis. Metabolic reactions that alter the rate of ATP utilization in animals include Na+, K+-ATPase and protein turnover. The concentration of Na+, K+-ATPase enzyme unites in skeletal muscle and liver of young adult obese (ob/ob) mice is lower than in tissues of young adult lean mice. There also appear to be alterations in protein turnover in certain tissues of obese (ob/ob) mice, but additional studies are required to determine if whole-body protein turnover is altered in these animals. Data are unavailable on either Na+, K+-ATPase or protein turnover in tissue of animals with dietary-induced thermogenesis. Continuation of studies in these areas should provide a metabolic basis for understanding individual variability in efficiency of energy retention.
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D001833:Body Temperature Regulation; D004032:Diet; D002149:Energy Intake; D004734:Energy Metabolism; D051379:Mice; D009765:Obesity / Q000235:genetics / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D011506:Proteins; D000254:Sodium-Potassium-Exchanging ATPase