Muscle Biology Laboratory, School of Kinesiology, Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Med Sci Sports Exerc. 2011 Jul;43(7):1148-53. doi: 10.1249/MSS.0b013e31820a7f65.
A single exercise bout stimulates skeletal muscle glucose transport (GT) in the absence or presence of insulin. It has been suggested that the kallikrein-kinin system may contribute to exercise effects on both insulin-independent and insulin-dependent GT. Plasma kininogen, a key kallikrein-kinin system component, is a protein substrate for the enzyme kallikrein and the source of the peptide bradykinin.
This study aimed to determine whether the postexercise (PEX) increase in insulin-dependent or insulin-independent GT is reduced in rats deficient in plasma kininogen versus normal rats.
Male Brown Norway (BN) and Brown Norway Katholiek (BNK; plasma kininogen-deficient) rats were studied. BN and BNK rats were assigned to exercise (4×30-min swim) or sedentary (SED) groups. Rats were anesthetized immediately (0hPEX) or 3 h (3hPEX) after exercise. For 0hPEX and 0hSED rats, one epitrochlearis muscle per rat was used for AMPK phosphorylation and muscle glycogen analyses. The contralateral muscle was incubated with [H]-3-O-methylglucose (3-MG) for GT assay. For 3hPEX and 3hSED rats, one muscle from each rat was incubated without insulin, and the contralateral muscle was incubated with 60 μU·mL insulin, and both muscles were incubated with 3-MG for GT measurement.
For 0hPEX versus 0hSED, both BN and BNK rats had greater insulin-independent GT and AMPK phosphorylation with reduced glycogen after exercise. No genotype effects were found 0hPEX. There was a significant main effect of exercise (3hPEX>3hSED) and no interaction between exercise and genotype for basal or insulin-stimulated GT.
Plasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation, or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX, suggesting that normal plasma kininogen is not essential for these important exercise effects.
本研究旨在确定与正常大鼠相比，血浆激肽原缺乏的大鼠在运动后（PEX）胰岛素依赖性或胰岛素非依赖性 GT 增加是否减少。
雄性棕色挪威（BN）和棕色挪威 Katholiek（BNK；血浆激肽原缺乏）大鼠进行了研究。BN 和 BNK 大鼠被分配到运动（4×30 分钟游泳）或静止（SED）组。大鼠在运动后立即（0hPEX）或 3 小时（3hPEX）麻醉。对于 0hPEX 和 0hSED 大鼠，每只大鼠的一只外展肌用于 AMPK 磷酸化和肌肉糖原分析。对另一侧肌肉进行 [H]-3-O-甲基葡萄糖（3-MG）摄取测定以测量葡萄糖转运（GT）。对于 3hPEX 和 3hSED 大鼠，每只大鼠的一只肌肉在无胰岛素孵育，对侧肌肉在 60μU·mL 胰岛素孵育，并用 3-MG 孵育测量 GT。
与 0hSED 相比，运动后 BN 和 BNK 大鼠的胰岛素非依赖性 GT 增加，AMPK 磷酸化增加，糖原减少。0hPEX 时未发现基因型影响。运动（3hPEX>3hSED）有显著的主效应，而运动和基因型之间没有交互作用，无论是基础状态还是胰岛素刺激状态下的 GT 都是如此。
血浆激肽原缺乏并未改变 0hPEX 时的胰岛素非依赖性 GT、AMPK 磷酸化或糖原耗竭，或 3hPEX 时的胰岛素依赖性 GT，表明正常的血浆激肽原对于这些重要的运动效应不是必需的。
