| Project/Area Number |
12672244
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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 |
Laboratory medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MIZUNO Akira The University of Tokushima, Medical School Hospital, Instructor, 医学部・附属病院, 助手 (80219641)
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| Co-Investigator(Kenkyū-buntansha) |
NOMA Yoshihiko The University of Tokushima, Medical School Hospital, Assistant Professor, 医学部・附属病院, 講師 (10218349)
KUWAJIMA Masamichi The University of Tokushima, School of Medicine, Associate Professor, 医学部, 助教授 (00205262)
村上 尚 徳島大学, 医学部, 助手 (40210009)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Insulin resistance / diabetes mellitus / liver cirrhosis / portal glucosensor / platelet / レプチン |
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| Research Abstract |
We examined insulin sensitivity in 60 patients with chronic liver disease using hyperinsulinemic euglycemic clamp method and our simplified method by platelet aggregation, because we noticed that insulin sensitivity in cirrhotic patients evaluated by simplified method using platelet was tend to be in normal in the other study. So we concluded that simplified method using platelet could reflect insulin resistance only in the peripheral tissues but not in the liver tissue. We found that the C-peptide (CPR) response to oral glucose load during hyperinsulinemic euglycemic clamp (clamp-OGL-CPR method) could evaluate the function of portal glucosensor (PGS). We measured CPR response in 30 diabetics, 10 obese subjects with IGT and 10 obese subjects with normal glucose tolerance and 10 normal subjects as control. The CPR response in the diabetics with or without obesity and obese subjects with IGT was remarkably reduced or completely absent nevertheless that in obese subjects without glucose intolerance (simple obesity) was good. CPR response in the patients with liver cirrhosis during clamp-OGL-CPR method was remarkably reduced like diabetic patient. We supposed that the disorders in PGS might be related to postprandial hyperglycemia not only in diabetics but also in the patients with liver cirrhosis, and could not relate to insulin resistance. Now we have been examining the relation between the function of PGS and the glucose intolerance in the animal model of type 2 diabetes. In other study, we made clear that leptin could increase insulin-stimulated glucose uptake in the peripheral tissues but not in liver tissue.
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