Regulation of contraction-induced FA uptake and oxidation by AMPK and ERK1/2 is intensity dependent in rodent muscle.

Regulation of contraction-induced FA uptake and oxidation by AMPK and ERK1/2 is intensity dependent in rodent muscle.
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AMPK 和 ERK1/2 对收缩诱导的 FA 摄取和氧化的调节在啮齿动物肌肉中具有强度依赖性。

DOI:
10.1152/ajpendo.00155.2006
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发表时间:
2006
期刊:
American journal of physiology. Endocrinology and metabolism
影响因子:
--
通讯作者:
Turcotte,LorraineP
Turcotte,LorraineP
中科院分区:
--
文献类型:
--
作者:
Raney,MarcellaA;Turcotte,LorraineP

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肌肉收缩激活AMP激活蛋白激酶(AMPK)和细胞外信号调节激酶(ERK 1/2),这两种信号分子参与肌肉代谢的调节。本研究的目的是确定AMPK和/或ERK 1/2的激活是否有助于调节肌肉脂肪酸(FA)的摄取和氧化在收缩肌肉。在休息(R)或通过操纵串持续时间(E1 = 25 ms,E2 = 50 ms,E3 = 100 ms,E4 = 200 ms)增加强度的电刺激(E)期间灌注大鼠后躯。对于匹配的FA输送,在E1、E2和E3期间,FA摄取显著大于R(分别为7.8 ± 0.7 vs. 14.4 ± 0.3、16.9 ± 0.8、15.2 ± 0.5 nmol·min-1·g-1,P< 0.05),但在E4期间则不是(8.3 ± 0.3 nmol·min-1·g-1,P> 0.05)。在E1和E2期间,FA氧化显著大于R(1.5 ± 0.1 vs. 2.3 ± 0.2,2.5 ± 0.2 nmol·min-1·g-1,P< 0.05),然后E3和E4恢复到静息水平(1.8 ± 0.1和1.5 ± 0.2 nmol·min-1·g-1,P> 0.05)。FA摄取与ERK 1/2从R到E3的磷酸化呈正相关(R2= 0.55,P < 0.05)以及FA氧化与ERK 1/2磷酸化之间的关系(R2= 0.76,P < 0.05),当E4和E3和E4的数据分别,纳入分析(R2= 0.04和R2 = 0.03,P> 0.05)。相关分析显示,在不同强度的运动中,FA摄取量与FA氧化量、AMPK活性均呈正相关(R2= 0.57,R2 = 0.65,P< 0.05)。这些结果,结合我们实验室以前的数据,表明ERK 1/2和AMPK是主要的信号分子调节FA摄取和氧化过程中的低到中等强度的肌肉收缩和中到高强度的肌肉收缩,分别。
Muscle contraction activates AMP-activated protein kinase (AMPK) and extracellular signal-regulated kinase (ERK1/2), two signaling molecules involved in the regulation of muscle metabolism. The purpose of this study was to determine whether activation of AMPK and/or ERK1/2 contributes to the regulation of muscle fatty acid (FA) uptake and oxidation in contracting muscle. Rat hindquarters were perfused during rest (R) or electrical stimulation (E) of increasing intensity by manipulating train duration (E1 = 25 ms, E2 = 50 ms, E3 = 100 ms, E4 = 200 ms). For matched FA delivery, FA uptake was significantly greater than R during E1, E2, and E3 (7.8 ± 0.7 vs. 14.4 ± 0.3, 16.9 ± 0.8, 15.2 ± 0.5 nmol·min−1·g−1, respectively,P< 0.05), but not during E4 (8.3 ± 0.3 nmol·min−1·g−1,P> 0.05). FA oxidation was significantly greater than R during E1 and E2 (1.5 ± 0.1 vs. 2.3 ± 0.2, 2.5 ± 0.2 nmol·min−1·g−1,P< 0.05) before returning to resting levels for E3 and E4 (1.8 ± 0.1 and 1.5 ± 0.2 nmol·min−1·g−1,P> 0.05). A positive correlation was found between FA uptake and ERK1/2 phosphorylation from R to E3 (R2= 0.55,P< 0.05) and between FA oxidation and ERK1/2 phosphorylation from R to E2 (R2= 0.76,P< 0.05), correlations that were not maintained when the data for E4 and E3 and E4, respectively, were included in the analysis (R2= 0.04 andR2= 0.03,P> 0.05). A positive correlation was also found between FA uptake and FA oxidation and AMPK activity for all exercise intensities (R2= 0.57,R2= 0.65 respectively,P< 0.05). These results, in combination with previous data from our laboratory, suggest that ERK1/2 and AMPK are the predominant signaling molecules regulating FA uptake and oxidation during low- to moderate-intensity muscle contraction and during moderate- to high-intensity muscle contraction, respectively.
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