| Budget Amount *help |
¥3,910,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Research Abstract |
We measured BMI, serum insulin, serum glucose, leptin, TNF alpha, GH and Adiponectin in obesity women and healthy volunteer. After the 3 month exercise program BMI. Serum insulin, serum glucose, leptin, and TNF alpha were significantly decreased compared with normal person, but GH and Adiponectin were decreased. We also measured MCT in pressured smooth muscle cells. Lactate is formed and utilized continuously under fully aerobic conditions. Lactate is oxidized actively at all times, especially during exercise. Family of monocarboxylate transport proteins (MCTs) that are differentially expressed in cells and tissues accomplishes the facilitated transport of lactate across membranes. Previously we reported that there is MCT1 in blood circulation. We also reported the pressure stress stimulated cell proliferation in aortic smooth muscle cells (HASMC). In this experiment we attempted to prove the existence of MCT1 in HASMC and to clarify the effect of pressure stress on MCT1 localization in HASMC. We determined succinate dehydrogenase (SDH) activity as a marker of energy metabolism in cells. SDH activity was increased by pressure stress. Lactate enhanced the SDH activity under pressure stress (160 mmHg for 3 hours) as dose dependent manner. On the other hand, lactate excretion was suppressed by the addition of lactate. We could detect MCT1 in the cytosolic and the membrane fractions of HASMC. The pressure stress increased MCT1 in the membrane fraction in the presence of extracellular lactate. In summary, we proved the existence of MCT1 in HASMC. Pressure stress changed the localization of MCT1. The increased membranous MCT1 may transport lactate for energy metabolism in cells.
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