| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Research Abstract |
We investigated the relationship between the cardiac function and the energy shift from free fatty acids (FFA) to glucose at a time of cardiac dysfunction using CD36 knockout (CD36KO) mouse, which is a transporter of FFA. The analysis of positron emission tomography revealed that the cardiac uptake of glucose was more increased in CD36KO mice compared with wild-type mouse, along with the overexpression of GLUT -1. By the metabolomics analysis, intracellular levels of acetyl CoA, long chain fatty acid (oleic acid, linoleic acid and palmitic acid), ATP and Phoshpocreatin were higher and the level of citric acid were lower in CD36KO mouse, suggesting that the de novo production of FFA originated from acetyl CoA might be increased. Analyzed by ultrasound cardiography, the heart in CD36KO mouse tended to be hypertropic. After the pressure overload by Thoracic Aortic Constriction (TAC), the weights of heart and lung were increased and the cardiac function got worse from the cardiac hypertrophy to the heart failure. In the heart of the CD36KO mouse, although phosphorylation of S6 ribosomal protein existed, neither apoptosis nor a vascular defect existed. These results suggested that the energy in thecardiomyocyte in CD36KO mouse was in the superfluous state, the energy state failed at an early stage from the state of cardiac hypertrophy to the heart failure when the pressure overload to the heart was performed.
|
