|Budget Amount *help
¥3,600,000 (Direct Cost : ¥3,600,000)
Fiscal Year 2002 : ¥1,400,000 (Direct Cost : ¥1,400,000)
Fiscal Year 2001 : ¥2,200,000 (Direct Cost : ¥2,200,000)
Introduction : Estrogen is a female steroid hormone, controlling various physiological functions. When the gene responsible for estrogen synthesis (Cyp19) was inactivated by targeting disruption in mice, various metabolic abnormalities including the obesity, fatty liver, and the insulin resistance of sugar metabolism were observed. This study is aiming to examine whether these phenotypes can be corrected not by the medicine but by exercise-load. Moreover, by combining exercise it was also examined whether the effect of the medicine prescribed for the mice could be reinforced. Result and Discussion : Exercise improve neither in glucose tolerance nor in insulin action in blood-glucose clearance test, significantly. Moreover, the mRNA levels of the acyl-CoA oxidase and catalase genes in the liver, and of the GLUT4 gene in muscles have not been improved by the exercise-load. However, mice treated both with exercise-load and with dietary fenofibrate, which is a hyperlipemia medicine, showed improvement in the insulin resistance phenotype of ArKO mice, when compared that of the mice loaded with exercise alone. These results demonstrate that although exercise alone does not improve the insulin resistance resulting from estrogen lack, it can reinforce the effects of the curative medicine. Clarification of molecular mechanisms underlying which exercise improves the abnormalities resulted from estrogen-insufficiency is a theme important to establish a cure with few side effects.