| Project/Area Number |
16590480
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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 |
Hygiene
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
MIURA Yoshikazu Dokkyo Medical University, School of Medicine, Hygiene, Associate Professor, 医学部, 助教授 (20049240)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2006: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Triphenyltin / Insulin secretion / Cytosolic Ca^<2+> / Cytosolic Na^+ / Membrane potential / ATP / ADP ratio / NADPH / Hamster / AChレセプター / GLPレセプター / SUR1 / 糖尿病 / インクレチン / ジアゾキシド / 高K^+ / ADP |
|---|
| Research Abstract |
Oral administration of a single dose of triphenyltin chloride (TPT) (60 mg/kg body wt) induces diabetes with decreased insulin secretion in hamsters.
The pathogenesis of triphenyltin-induced diabetes in hamster involves 1) the glucose-induced reduction of [Ca^<2+>]_i and insulin secretion in response to ATP-sensitive K^+ channel-dependent depolarization, which is related to the decrease of NADPH and ATP or ATP/ADP ratio in pancreatic islet cells, 2) the reduction of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like-peptide-1 (GLP-1)-induced Na^+-dependent cellular Ca^<2+> response through PKA-dependent and PKA-independent mechanisms in pancreatic islet cells (Ref. 1). Triphenyltin induces the increase of high K^+ and torbutamide-induced [Ca^<2+>]_i and insulin secretion and increases the ATP-sensitive K^+ channel-independent insulin secretion in islet cells.
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