| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Research Abstract |
The objective of this study was to investigate the effect and its mechanisms of various selenium status and/or ingestion of selenocompounds on the development of diabetes mellitus. The supplementation of sodium selenite (Na_2SeO_3) resulted in the decrease of blood glucose and the increase of plasma insulin after oral glucose tolerance test in type 2 diabetes model NSY mice. As the possible candidates effective for glucose torelance, Na_2SeO_3, methyl seleninic acid and seleno-L-methionine (SeMet) were administered to streptozotocin/nicotinamide-induced short-term diabetic mouse model, and the results indicated that SeMet was most effective against glucose intolerance. The effect is presumably related to increased selenium content and glutathione peroxidase 1 (GPX1) mRNA expression and suppressed ROS production in pancreas, and decreased free fatty acid (FFA) and HbA1C levels and increased adiponectin level in plasma. SeMet accelerated glucose uptake by phosphatidylinositol-3-kinase activation through the suppression of ROS production that was linked to the control of insulin receptor substrate phosphorylation in 3T3-L1 adipocytes. The glycogen storage lowered by treatment of palmitate as FFA in Hepa 1-6 cells was recovered by SeMet until the normal level. These results suggest that SeMet exhibits the improving effects against insulin resistance by promoting insulin signaling in adipocytes and hepatocytes through the suppression of ROS production because the selenocompound predominantly enhances GPX1 expression in both cells.
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