2000 Fiscal Year Final Research Report Summary
Study of mechanism of potentiation of insulin sensitivity during exercise-bradykinin induced glucose uptake in muscle
| Project/Area Number |
10671078
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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 |
Metabolomics
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| Research Institution | KUMAMOTO UNIVERSITY MEDICAL SCHOOL |
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Principal Investigator |
KISHIKAWA Hideki KUMAMOTO UNIVERSITY MEDICAL SCHOOL, LECTUROR, 医学部, 講師 (30161441)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMURA Nobuhiro KUMAMOTO UNIVERSITY MEDICAL SCHOOL, RESEARCH ASSISTANT, 医学部・附属病院, 助手 (40274716)
ARAKI Eiichi KUMAMOTO UNIVERSITY MEDICAL SCHOOL, PROFESSOR, 医学部, 教授 (10253733)
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| Project Period (FY) |
1998 – 2000
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| Keywords | DIABETES MELLITUS / EXERCISE / BRADYKININ / INSULIN SENSITIVITY |
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| Research Abstract |
The bradykinin receptor binding and RT-PCR studies revealed that dog skeletal muscle and L6 myoblats possessed significant numbers of bradykinin receptor (type2). Bradikinin significantly increased glucose uptake in isolated dog muscle and L6 myoblasts in the presence of insulin in a dose-dependent manner. In human studies, plasma bradykinin concentrations increased significantly during exercise in healthy subjects and well-controlled type 2 diabetic patients but not in poorly controlled type 2 diabetic patients. In rat studies, plasma bradykinin concentrations also significantly increased after swimming in nondiabetic and mildly diabetic rats, but not in rats with severe diabetes. GLUT-4 translocation in skeletal muscle of nondiabetic rats significantly increased after swimming, but these increases were abrogated by subcutaneous infusion of bradykinin B2 receptor antagonists. In conclusion, it was suggested that plasma bradykinin concentrations could increase in response to acute exercise and this increase was affected by blood glucose status in diabetic patients, and that the exercise-induced increase in bradykinin might be involved in modulating exercise-induced glucose transport through an increase of GLUT-4 translocation.
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