| Project/Area Number |
13671207
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
SHOJI Shingo Kurume University School of Medicine, Department of Endocrinology and Metabolism, Assistant Professor, 医学部, 講師 (10281528)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Syusuke Kurume University School of Medicine, Department of Endocrinology and Metabolism, Research Assistant, 医学部, 助手 (60268943)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Hypoglycemic Rat / Neuronal Adaptation / Monocarbonic Acid Transporter (MCT) / グリコーストランスポーター / 低血糖ラット / 低血糖の急性適応 / 低血糖の慢性適応 / グルコーストランスポーター |
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| Research Abstract |
To evaluate the role of monocarbonic acid transporter on the glucose sensitiveness of excitable transmission in the central nervous system, we performed optical technique by using photo-sensitive dye in the first year. Bath application of low glucose (2 mM) artificial cerebral fluid induced suppression (60%) of the transmission by electrical stimulation within 10 minutes in the septal nucleus or hippocampus of the fresh brain slices of normal rats. Pre-application of low glucose solution decreased the suppression (20%) of the transmission by low glucose solution in the same period of time (Acute adaptation against hypoglycemia). This adaptation was shown in monocarbonic acid transporter inhibitor containing solution. When the low glucose solution was exchanged to the normal solution, recovery time from suppression of neural excitability was prolonged one and half times in the MCT inhibitor containing solution. The suppression of neural excitability in the slices of chronic hypoglycemic
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rats made by 7 days subcutaneous NPH-insulin injection was smaller (30%) in comparison with the slices of normal rats (Chronic adaptation against hypoglycemia). In the MCT inhibitor containing solution, this adaptation was partially attenuated in the slices of the chronic hypoglycemic rats. These data suggest that MCT might modulate the recovery from suppression of neuronal excitability by hypoglycemia and the sensitivity to hypoglycemia in the chronic hypoglycemic rats. In the second year, by using the Northern blot analysis, we measured expression amount of MCT1-, MCT2-RNA. In the normal rat brain, no MCT1- and MCT2-RNA were expressed. However both MCT1- and MCT2-RNA were expressed in the chronic hypoglycemic rat brain at the same amount. In the normal rat brain pretreated with low glucose solution, MCT1- and MCT2-RNA were slightly expressed. By using Western blot analysis with anti-MCT1- and anti-MCT2 antibody, we analyzed the expression of MCT1- and MCT2-protein in the brain of the normal rats and the chronic hypoglycemic rats. In the normal rat brain, no MCT1- and MCT2-protein were expressed. In the chronic hypoglycemic rat brain, both MCT1- and MCT2-protein were highly expressed at the same degree. These data suggest that expression of MCT might be increased in the brain by exposure of hypoglycemia and that increase of MCT function might modulate the adaptation of neuronal excitability against hypoglycemic condition. Less
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