Abstract. lifestyle-related diseases are associated with overeating and lack of exercise. the purpose of this study was to investigate the effect of exercise and high-fat diet on plasma adiponectin and nesfatin levels. mice were housed for 4 weeks in 4 groups, which included the non-exercise and normal diet (Sn), exercise and normal diet (En), non-exercise and high-fat diet (SF) and the exercise and high-fat diet (EF) group. the mice in the exercise groups were housed in cages with a running wheel and were subjected to voluntary exercise. the food intake (Kcal) of the mice in the exercise groups increased compared to that of the mice in the non-exercise groups (p<0.01). Body weight and visceral fat decreased in the mice in the EF group compared to the mice in the SF group (p<0.01 and p<0.05). the temperature of the mice in the EF group increased compared to that of the mice in the Sn group (p<0.05). Blood glucose, insulin (p<0.01), cholesterol (p<0.01) and triglyceride concentrations (p<0.01) increased in the SF group compared to the normal diet groups. Furthermore, plasma insulin and cholesterol concentrations increased in the SF group compared to the exercise groups (p<0.01). plasma adiponectin and nesfatin-1 levels in the SF group decreased compared to the Sn group (p<0.05). Exercise under a high-fat diet antagonized the significant decrease in the nesfatin-1 level. Exercise together with a high-fat diet affected the plasma levels of adiponectin and nesfatin. it is therefore suggested that exercise together with a high-fat diet can affect various diseases via adiponectin and nesfatin.

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Endocrine disruption during gestation impairs the physical and behavioral development of offspring. However, it is unclear whether endocrine disruption also impairs maternal behavior and in turn further contributes to the developmental and behavioral dysfunction of offspring. We orally administered the synthetic non-steroidal estrogen diethylstilbestrol (DES) to pregnant female C57BL/6J mice from gestation day 11–17 and then investigated the maternal behavior of mothers. In addition, we examined the direct effects of in utero DES exposure and the indirect effects of aberrant maternal behavior on offspring using the cross-fostering method. In mothers, endocrine disruption during gestation decreased maternal behavior. In addition, endocrine disruption of foster mother influenced anxiety-related behavior and passive avoidance learning of pups regardless of their exposure in utero. The influence of DES exposure in utero, irrespective of exposure to the foster mother, was also shown in female offspring. These results demonstrate the risks of endocrine disruptors on both mother as well as offspring and suggest that developmental deficits may stem from both in utero toxicity and aberrant maternal care.