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冲刺运动是否是人类骨骼肌中的瘦素信号模拟物?

Is sprint exercise a leptin signaling mimetic in human skeletal muscle?

机构信息

Department of Physical Education, University of Las Palmas de Gran Canaria, Spain.

出版信息

J Appl Physiol (1985). 2011 Sep;111(3):715-25. doi: 10.1152/japplphysiol.00805.2010. Epub 2011 Jun 9.

DOI:10.1152/japplphysiol.00805.2010
PMID:21659488
Abstract

This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.

摘要

这项研究旨在确定冲刺运动是否会激活与人类骨骼肌中瘦素作用相关的信号级联,以及这种激活模式如何受到葡萄糖摄入的干扰。15 名年轻健康男性随机分为两组,分别在空腹(n=7,C 组)和葡萄糖组(n=8,G 组)条件下进行 30 秒冲刺运动(Wingate 测试),并在运动前 1 小时摄入 75g 葡萄糖。运动后恢复期,葡萄糖摄入对 JAK2、STAT3、STAT5、ERK1/2、p38 MAPK 磷酸化和 SOCS3 蛋白表达的激活模式有不同的影响。与对照冲刺相比,控制冲刺后 30 分钟,STAT3 和 ERK1/2 磷酸化水平增加(均 P<0.05)。对照冲刺后 120 分钟,SOCS3 蛋白表达增加,但 PTP1B 蛋白表达不受影响。对照冲刺后 30 和 120 分钟,STAT5 磷酸化增加(P<0.05)。葡萄糖抑制了 30 分钟时的 STAT3 和 ERK1/2 磷酸化以及 120 分钟时的 SOCS3 蛋白表达增加,同时延缓了 STAT5 对冲刺的反应。尽管冲刺后循环瘦素浓度降低,但这些信号级联仍被激活。运动前摄入葡萄糖可降低基础 JAK2 和 p38 MAPK 磷酸化水平,并增加其磷酸化水平(均 P<0.05)。在恢复期间,当运动前摄入葡萄糖时,JAK2 磷酸化不变,p38 MAPK 磷酸化短暂降低。总之,空腹状态下进行的冲刺运动是人类骨骼肌中瘦素信号的模拟物。

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