2003 Fiscal Year Final Research Report Summary
mechanism of insulin autoantibody production for pathogenesis of pancreatic beta cell destruction and hyperplasia
| Project/Area Number |
13670478
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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 |
内科学一般
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
UCHIGATA Yasuko TWMU, Dept.of Medicine, Associate Prof., 医学部, 助教授 (50193884)
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| Co-Investigator(Kenkyū-buntansha) |
IWAMOTO Yasuhiko TWMU, Dept.of Medicine, Professor, 医学部, 教授・所長 (60143434)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Insulin autoantibody / Insulin autoimmune syndrome / Type 1 diabetes / Scatchard analysis / Insulin antibody |
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| Research Abstract |
Both of insulin autoimmune syndrome (IAS) and type 1 diabetes are characterized by insulin autoantibody. On the other hand, insulin antibody or anti-insulin antibody is a antibody against insulin which is injected subcutaneously. The insulin antibody and the insulin autoantibody have both an ability to bind insulin in human serum. Since reported by Hirata in 1970, we collected 244 patient record with insulin autoimmune syndrome (IAS) in Japan until 1997, which showed a development of averaged 9 patients with IAS per year. We collected 11 patients with IAS from 1998 to 1999, and collected 19 patients with IAS from 2000 to 2003. There was no increase of the development of IAS. Total of 274 patients with insulin autoimmune syndrome were collected in the end of 2003. Thirty-eight % of them was treated with sulfhydroxy compounds such as Methimazole, Thiola and Tathione before the development of IAS. According to the incidence of IAS, there was no increase year by year. Some of the patients had postprandial hyperglycemia after the development of IAS. the outcome of glucose tolerance test (GTT) was collected. Among them who were performed GTT, 59% had diabetic pattern, 38% had IGT pattern. It suggests that approximately 90% showed abnormal glucose metabolism. The characterization of the insulin autoantibody was done by Scatchard analysis using 125 I-human insulin. A major part of the insulin autoantibody was a high affinity (k1)-low capacity (b1) site, the site was compared with that of insulin antibody which were found in insulin-treated diabetic patients. The k1 and b1 were more than 1x10^8 L/mol and around 1 or less than 1x10^8 mol/L, respectively in insulin-treated diabetic patients, whereas those were less than 1x10^8 L/mol and more than 1x10^8 mol/L, respectively in the patients with IAS. There was a significant difference (p<0.001).
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