Project/Area Number |
10671075
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | The University of Tokushima |
Principal Investigator |
NOMA Yoshihiko The University of Tokushima, Medical School of Hospital, Assistant professor, 医学部・附属病院, 講師 (10218349)
|
Co-Investigator(Kenkyū-buntansha) |
MIZUNO Akira The University of Tokushima, Medical School of Hospital, Instructor, 医学部・附属病院, 助手 (80219641)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | microangiopathy / islet / diabetes mellitus / 糖尿病性血管障害 / 毛細血管微小血流 / OLETF |
Research Abstract |
The changes of capillary in islet and beta cells of spontaneity diabetes mellitus model OLETF rat (Otsuka Long Evans Fatty) were observed with confocal microscope. Then, the cause of the capillary change and its participation in the onset and aggravation of diabetes were analyzed. It was clarified that capillary in islet began to expand at eight weeks old when the insulin resistance began to appear, presented an eminent expansion at the onset of diabetes mellitus, and became narrow scarce after diabetes mellitus had developed. The density and the diameter of the capillary plexus were not distinguishable from the control at the border of islet where the insulin staining was excellent, but the dilatation of capillary was remarkable at the inner region. In addition, the capillary was narrow and scarce in the central part of islet. In addition, the minute flow that was thought to be canaliculi were not seen in the region where capitally was dilated or narrowed. The disturbance of inflow to canaliculi was thought to influence the islet function. The structural change that was common in microangiopathy was observed in the capillary of islet. In the islet after hyperglycemia had continued, small β cell clusters that were poor of capillary and the capillary network where the β cell did not exist were observed. Though it seems to exist enough amount of beta cells in the expanded islet of OLETF pancreas at the onset of diabetes, there were a lot of parts of the blood flow insufficiency by the capillary changes of islet and, therefore, it was thought that only a part of 6 cell area was effective with enough blood flow. We tried to protect capillary changes to prevent the depression of beta cell function. The insulin resistance was improved by the drug and the effectiveness of preventing beta cell function by direct protection of capillary dilatation.
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