Insulin and exercise differentially regulate PI3-kinase and glycogen synthase in human skeletal muscle
Insulin and exercise differentially regulate PI3-kinase and glycogen synthase in human skeletal muscle
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DOI：
10.1152/jappl.2000.89.4.1412
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发表时间：
2000-10-01
影响因子：
3.3
通讯作者：
Kirwan, JP
中科院分区：
文献类型：
--
作者：
O'Gorman, DJ;Del Aguila, LF;Kirwan, JP
本研究旨在探讨运动和胰岛素单独及联合作用对活体人骨骼肌磷脂酰肌醇3-激酶(PI3-K)和糖原合成酶活性的影响。七名健康男性按随机顺序进行了三次试验。这些试验包括：1)在10%的溶液中摄入2g/kg体重的碳水化合物(CHO)；2)75min的半卧位自行车运动，最大氧耗量的75%；然后是5x1分钟的最大冲刺(Ex)；以及(3)Ex，紧接着摄入碳水化合物溶液(ExCHO)。在CHO和ExCHO期间，血糖和胰岛素在试验后15分钟和30分钟(15分钟后和30分钟后)均升高(P<；0.05)，尽管ExCHO组的胰岛素水平较低。CHO和ExCHO恢复期间的高胰岛素血症导致PI3-激酶活性在30后较基础水平升高(P<；0.001)，尽管ExCHO的增幅较低(P<；0.004)。此外，在Ex和ExCHO期间，PI3-激酶活性在运动后即刻(Post-0)受到抑制(P<；0.02)。所有试验的胰岛素反应曲线下面积与PI3K活性呈正相关(r=0.66P<；0.001)。糖原合成酶活性在CHO期间没有增加，但在Ex和ExCHO期间在0后和30后显著增加(P<；0.05)。在CHO和ExCHO期间，摄入饮料增加了碳水化合物的氧化(P<；0.05)，尽管ExCHO后的增加低于CHO(P<；0.05)。在所有试验中，碳水化合物氧化与PI3K活性直接相关(r=0.63P<；0.001)。总之，在静息条件下，摄入碳水化合物溶液会导致PI3-激酶途径的激活和碳水化合物的氧化。然而，当大强度运动后摄入碳水化合物时，PI3-激酶反应减弱，糖原合成酶活性增强，从而促进碳水化合物的非氧化代谢或储存。糖原合成酶的激活不依赖于PI3-激酶。
The purpose of this study was to determine the separate and combined effects of exercise and insulin on the activation of phosphatidylinositol 3-kinase (PI3-kinase) and glycogen synthase in human skeletal muscle in vivo. Seven healthy men performed three trials in random order. The trials included 1) ingestion of 2 g/kg body wt carbohydrate in a 10% solution (CHO); 2) 75 min of semirecumbent cycling exercise at 75% of peak O-2 consumption; followed by 5 x 1-min maximal sprints (Ex); and 3) Ex, immediately followed by ingestion of the carbohydrate solution (ExCHO). Plasma glucose and insulin were increased (P < 0.05) at 15 and 30 (Post-15 and Post-SO) min after the trial during CHO and ExCHO, although insulin was lower for ExCHO. Hyperinsulinemia during recovery in CHO and ExCHO led to an increase (P < 0.001) in PI3-kinase activity at Post-30 compared with basal, although the increase was lower (P < 0.004) for ExCHO. Furthermore, PI3-kinase activity was suppressed (P < 0.02) immediately after exercise (Post-0) during Ex and ExCHO. Area under the insulin response curve for all trials was positively associated with PI3-kinase activity (r = 0.66, P < 0.001). Glycogen synthase activity did not increase during CHO but was increased (P < 0.05) at Post-0 and Post-30 during Ex and ExCHO. Ingestion of the drink increased (P < 0.05) carbohydrate oxidation during CHO and ExCHO, although the increase after ExCHO was lower (P < 0.05) than CHO. Carbohydrate oxidation was directly correlated with PI3-kinase activity for all trials (r = 0.63, P < 0.001). In conclusion, under resting conditions, ingestion of a carbohydrate solution led to activation of the PI3-kinase pathway and oxidation of the carbohydrate. However, when carbohydrate was ingested after intense exercise, the PI3-kinase response was attenuated and glycogen synthase activity was augmented, thus facilitating nonoxidative metabolism or storage of the carbohydrate. Activation of glycogen synthase was independent of PI3-kinase.