ENHANCED PERIPHERAL AND SPLANCHNIC INSULIN SENSITIVITY IN NIDDM MEN AFTER SINGLE BOUT OF EXERCISE
ENHANCED PERIPHERAL AND SPLANCHNIC INSULIN SENSITIVITY IN NIDDM MEN AFTER SINGLE BOUT OF EXERCISE
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DOI：
10.2337/diabetes.36.4.434
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发表时间：
1987-04-01
期刊：
影响因子：
7.7
通讯作者：
HORTON, ES
中科院分区：
文献类型：
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作者：
DEVLIN, JT;HIRSHMAN, M;HORTON, ES
我们研究了葡萄糖代谢的非胰岛素依赖型糖尿病（NIDDM）男性和无糖原消耗周期运动12小时前，并比较了我们以前的数据在瘦和肥胖的主题。总葡萄糖利用率、葡萄糖氧化率、非氧化葡萄糖处置率（NOGD）、葡萄糖代谢清除率（MCR）和内源性葡萄糖产生率（EGP）用“两水平”胰岛素钳夹技术（40和400 mU输注100分钟）测定。m-2.cntdot. min ~（-1）联合间接量热法和D-3-[~ 3 H]葡萄糖输注。在胰岛素输注前后，分析股外侧肌肌活检标本的糖原含量和糖原合成酶活性。运动后，NIDDM受试者的肌糖原浓度与瘦和肥胖受试者相当。先前运动和胰岛素输注的糖原合成酶的激活与瘦对照相似。运动后，总葡萄糖处置在40-mU. cntdot期间显著增加。m-2.cntdot. min-1输注（P <0.05），但在400-mU. m-2.cntdot. min-1输注无显著性差异。运动后的这些增加是两种胰岛素输注水平期间NOGD显著升高的结果。与瘦型受试者相比，NIDDM患者在两次胰岛素输注期间的葡萄糖MCR均降低，但与肥胖非糖尿病患者非常相似。基础EGP在运动后的早晨显著降低（4.03 . ±. 0.27对比3.21 .+-。0.21 mg. cntdot。kg-1去脂质量。min-1）（P <0.05），并与空腹血糖（197 . ± 0.05）显著降低相关。12对164 +-。9毫克/分升）。通过40-mU抑制EGP m-2.cntdot. min-1输注量在运动后早晨也更大（54 vs. 90%的基础）（P <0.05）。这项研究表明，一个单一回合的糖原消耗运动显着增加外周和内脏胰岛素敏感性12-16小时后，在NIDDM男性。运动后外周葡萄糖利用率的增加是NOGD增加的结果，可能反映了葡萄糖作为糖原储存的增加。运动后胰岛素刺激的葡萄糖氧化速率降低。运动后较低的空腹血糖浓度是由于EGP减少而不是葡萄糖利用增加。
We studied glucose metabolism in non-insulin-dependent diabetic (NIDDM) men with and without glycogen-depleting cycle exercise 12 h beforehand and have compared the results to our previous data in lean and obese subjects. Rates of total glucose utilization, glucose oxidation, nonoxidative glucose disposal (NOGD), glucose metabolic clearance rate (MCR), and endogenous glucose production (EGP) were determined with a "two-level" insulin-clamp technique (100-min infusions at 40 and 400 mU .cntdot. m-2 .cntdot. min-1) combined with indirect calorimetry and D-3-[3H]glucose infusion. Muscle biopsy specimens from vastus lateralis were analyzed for glycogen content and glycogen synthase activity before and after insulin infusion. After exercise, NIDDM subjects had muscle glycogen concentrations comparable with those of lean and obese subjects. The activation of glycogen synthase both by prior exercise and insulin infusion was similar to lean controls. After exercise, total glucose disposal was significantly increased during the 40-mU .cntdot. m-2 .cntdot. min-1 infusion (P < .05), but the increase observed during the 400-mU .cntdot. m-2 .cntdot. min-1 infusion was not significant. These increases after exercise were the result of significantly higher NOGD during both levels of insulin infusion. The MCR of glucose during both insulin infusions was reduced in NIDDM compared with lean subjects but was very similar to that in obese nondiabetics. Basal EGP was significantly reduced on the morning after exercise (4.03 .+-. 0.27 vs. 3.21 .+-. 0.21 mg .cntdot. kg-1 fat-free mass .cntdot. min-1) (P < .05) and associated with signmificant reductions of fasting plasma glucose (197 .+-. 12 vs. 164 .+-. 9 mg/dl). Suppression of EGP by the 40-mU .cntdot. m-2 .cntdot. min-1 infusion was also greater on the morning after exercise (54 vs. 90% of basal) (P < .05). This study demonstrates that a single bout of glycogen-depleting exercise significantly increases peripheral and splanchic insulin sensitivity 12-16 h later in NIDDM men. Increased peripheral glucose utilization after exercise is the result of increased NOGD, presumably reflecting increased glucose storage as glycogen. Insulin-stimulated rates of glucose oxidation are decreased after exercise. The lower fasting glucose concentration after exercise is due to decreased EGP rather than increased glucose utilization.