1998 Fiscal Year Final Research Report Summary
PATHOLOGICAL RESEARCH OF DIABETIC COMPLICATION OF SPONTANEOUS DIABETIC RAT (WBN/Kob)
| Project/Area Number |
09660347
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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 |
Applied veterinary science
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| Research Institution | SETSUNAN UNIVERSITY |
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Principal Investigator |
NARAMA Isao FACULTY OF PHARMACEUTICAL SCIENCE,SETSUNAN UNIVERSITY PROFESSOR, 薬学部, 教授 (80268490)
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| Co-Investigator(Kenkyū-buntansha) |
OZAKI Kiyokazu FACULTY OF PHARMACEUTICAL SCIENCE,SETSUNAN UNIVERSITY RESEARCHER, 薬学部, 研究員 (40268496)
MATSUURA Tetsuro FACULTY OF PHARMACEUTICAL SCIENCE,SETSUNAN UNIVERSITY RESEARCHER, 薬学部, 研究員 (20268494)
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| Project Period (FY) |
1997 – 1998
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| Keywords | DIABETES MELLITUS / DIABETIC COMPLICATION / PATHOLOGY / ANIMAL MODEL |
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| Research Abstract |
1. Autonomic nerve lesion of WBN/Kob rat
Autonomic nerve lesion of spontaneous diabetic WBN/Kob rats is characterized by axonal dystrophy and miniaturization of axon diameter in mesenteric ganglion. These changes are similar to that of human diabetic autonomic neuropathy. Peripheral motor neuropathy of WBN/Kob rat is segmental demyelination. These findings confirmed pathogenesis of peripheral motor neuropathy in WBN/Kob rat is different from that of autonomic neuropathy. However, axon of ileal, colonic, cecal, and vagus nerve increased in size and have no axonal dystrophy. Therefore, it was indicated the influences of diabetes is weak in ileal, colonic, cecal, and vagus nerve.
2. Muscle lesion of WBN/Kob rat
Despite peripheral nerve abnormalities in WBN/Kob rats, neurogenic abnormality was not seen in muscles.Morphometric analysis of myofiber size by fiber type indicated severe atrophy of type 2a myofibers in extensor digitorum longus muscle, biceps femoris muscle, soleus muscle and diaphragm, hyperirophy of type 2b myofibers in extensor digitorum longus muscle and diaphragm, and hypertrophy of type 1 myofiber in biceps femoris muscle. These changes diffcrcd from age-dependent changes. It may be caused by the diabetic dysmetabolism of anaerobic glycolysis.
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