| Project/Area Number |
11480005
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
体育学
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| Research Institution | University of Tsukuba, Institute of Health and Sport Sciences |
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Principal Investigator |
TOKUYAMA Kumpei University of Tsukuba, Institute of Health and Sport Sciences, Associate Professor, 体育科学系, 助教授 (00207565)
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| Co-Investigator(Kenkyū-buntansha) |
NAGASAKA Shoichiro Jichi Medical School, Assistant Professor, 講師 (00296112)
KIYONAGA Akira University of Tsukuba, Institute of Health and Sport Sciences, Professor, 体育学部, 教授 (70177955)
TANAKA Hiroaki University of Tsukuba, Institute of Health and Sport Sciences, Professor, 体育学部, 教授 (00078544)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1999: ¥9,800,000 (Direct Cost: ¥9,800,000)
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| Keywords | minimal model / insulin sensitivity / glucose sensitivity / endurance exercise / 糖負荷試験 / 運動トレーニング / 同位体標識糖 / 糖尿病 / 運動療法 / 安定同位体 / 肝糖放出 / 長距離走者 |
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| Research Abstract |
Glucose itself can enhance glucose disposal and suppress production independent of a change in insulin. Although literature abounds with reports of effect of exercise on insulin sensitivity (SI), there is a paucity of literature relating to the effect of physical exercise on glucose effectiveness. We have studied pathogenesis of glucose intolerance and beneficial effects of exercise on glucose effectiveness (SG) by minimal model approach, which is a mathematical model to analyze time course of glucose and insulin during intravenous glucose tolerance test. Although there was a heterogeneity in SI and pancreatic insulin secretion in subjects with impaired-glucose tolerance (IGT) and non insulin dependent diabetes mellitus (NIDDM), at least one of the two is reduced resulting in reduced insulin action. Decreased SG was common hi IGT and NIDDM subjects regardless of their insulin sensitivity index. Furthermore, adopting stable-labeled glucose enabled us to isolate peripheral component of SI (SI^<2*>) and SG (SG^<2*>) and both indexes are enhanced in endurance trained subjects. Endogenous glucose production (EGP) of NIDDM patients was suppressed but it was less than that of controls suggesting that hepatic glucose effectiveness specific to suppressing EGP is decreased in NIDDM. In endurance trained athletes, EGP at basal condition was enhanced, is suppressed similarly during the first 30 min of IVGTT, recovered faster and overshot greater than those of control subjects. SG^<2*> and basal EGP positively correlate. The higher basal EGP and greater EGP-overshoot of endurance trained athletes function to compensate for the higher peripheral glucose demand in order to maintain glucose homeostasis.
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