| Project/Area Number |
07671128
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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 |
内分泌・代謝学
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ISHIDA Hitoshi Associate Professor, Department of Metabolism and Clinical Nutrition, Kyoto University School of Medicine, 医学研究科, 助教授 (80212893)
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| Co-Investigator(Kenkyū-buntansha) |
SEINO Yutaka Professor, Depatment of Metabolism and Clinical Nutrition, Kyoto University Scho, 医学研究科, 教授 (40030986)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Diabetes mellitus / Pancreatic beta-cells / Insulin secretion / Patch-clamp technique / ATP-sensitive K^+ channels / Voltage-dependent Ca^<2+> channels / Intracellular Ca^<2+> / パッチクランプ法 / 細胞内カルシウム濃度 |
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| Research Abstract |
As one of the major characteristics in pathophysiological aspects in noninsulin-dependent diabetes mellitus (NIDDM), the selective impairment of glucose-induced insulin secretion has been well known. On the other hand, the insulin secretory capacity is rather enhanced in response to the stimuli other than glucose. We, therefore, investigated the activity of voltage-dependent Ca^<2+> channel (VDCC) directly using the patch-clamp technique, which has a very important role on the regulation of intracellular Ca^<2+> levels. Using single beta-cells obtained by the dispersion of pancreatic islets of GK rats with genetically NIDDM,the L-and T-types of Ca^<2+> channel currents were recorded by whole cell recording. In addition, in order to investigate the intracellular mechanisms for modulating VDCC activities throuph glucose metabolism without mediating the K_<ATP> channel closure, the perforated patch using nystatin method was also utilized. Both of L-and T-type VDCC activities were found to be significautly enhanced after the membr anedepolarization in GK beta-cells when compared to the controls. In control beta-cells, the VDCC activities were more augmented after glucose loading in perforated patches. However, such an augmentation was not to be found in GK beta-cells. These phenomena seem to be closely related to the glucose selectivity of the impairment of insulin secretory capacity found in NIDDM beta cells of GK rats.
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