Effect of Exercise Training on Glucose Effectiveness Assessed by 2-compartment labelled minimal moelel

葡萄糖本身可以促进葡萄糖的处理和抑制产生，而不依赖于胰岛素的变化。尽管有关运动对胰岛素敏感性(SI)影响的文献很多，但有关运动对血糖有效性影响的文献却很少。我们用最小模型法研究了葡萄糖耐量异常的发病机制和运动对葡萄糖效能的有益影响。尽管糖耐量受损(IGT)和非胰岛素依赖型糖尿病(NIDDM)患者的SI和胰腺胰岛素分泌存在异质性，但两者中至少有一种是减少的，从而导致胰岛素作用减弱。血糖降低在IGT和NIDDM患者中很常见，无论他们的胰岛素敏感性指数如何。此外，采用稳定标记的葡萄糖使我们能够分离出SI和SG的外周成分，并且这两个指标在耐力训练的受试者中都得到了提高。NIDDM患者的内源性葡萄糖生成(EGP)受到抑制，但低于对照组，提示NIDDM患者肝脏葡萄糖抑制EGP的特异性降低。耐力训练运动员在基础状态下EGP增强，在IVGTT的前30min受到类似的抑制，恢复较快，超调量大于对照组。SG^&lt；2*&gt；与基础EGP呈正相关。耐力训练运动员较高的基础EGP和较大的EGP超调，其功能是补偿较高的外周葡萄糖需求，以维持葡萄糖稳态。

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.