1999 Fiscal Year Final Research Report Summary
インスリン感受性からみたインスリン非依存型糖尿病の成因に関する遺伝学的研究
Project/Area Number |
10470234
|
Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Tokyo Women's Medical University |
Principal Investigator |
IWAMOTO Yasuhiko Department of Medicine, Tokyo Women's Medical University Professor, 医学部, 教授 (60143434)
|
Co-Investigator(Kenkyū-buntansha) |
OGATA Makiko Department of Medicine, Tokyo Women's Medical University Assistant, 医学部, 助手 (10233404)
SUKURA Hiroshi Department of Medicine, Tokyo Women's Medical University Lecturer, 医学部, 講師 (70240710)
IWASAKI Naoko Department of Medicine, Tokyo Women's Medical University Lecturer, 医学部, 講師 (70203370)
|
Project Period (FY) |
1998 – 1999
|
Keywords | type 2 diabetes mellitus / insulin resistance / insulin sensitizer / PC-1 / PPAR-γ / affected sib-pair analysis / MODY |
Research Abstract |
1. Tyrvosine kinase inhibitor PC-1 and insulin resistance : The mean PC-1 activity of the cultured dermal fibroblasts from NIDDM patients was significantly higher than that of non-diabetic control subjects. 2. Serum leptin level as an indicator to predict the clinical efficacy of troglitazone (TRO) in patients with NIDDM : We investigated the relationship between serum leptin levels and clinical efficacy of TRO in 45 NIDDM patients. Reduction in FPG after TRO treatment was correlated with serum leptin and HOMA-R (insulin resistance index) at baseline, suggesting that serum leptin level at baseline control could be an useful indicator to predict the clinical efficacy of TRO in NIDDM. 3. Polymorphism of PPAR-γand insulin resistance : Polymorphism of PPAR-γgene (Pro 12 Ala) was not correlated with insulin resistance or the clinical efficacy of insulin sensitizer. 4. A genome-wide screen for type 2 diabetes susceptibility genes has been carried out in 270 affected sibpairs of type 2 diabetes, and 6 loci have been identified. 5. Clinical characteristics of juvenile-onset type2 diabetes and genetic background : We investigated the mutatins in the HNF-1β(MODY5) and A to G mutation at nucleotide 3243 of the mitochondrial (mt) DNA in 54 juvenile-onset diabetic patients who had started kidney diialysis under 50 years of age. Six patients had 3243 mutation of mt DNA, suggesting that the mutation has a greater effect on the progression of diabetic nephropathy.
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Research Products
(4 results)