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首页> 外文期刊>American Journal of Physiology >Regulation of contraction-induced FA uptake and oxidation by AMPK and ERK1/2 is intensity dependent in rodent muscle.
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Regulation of contraction-induced FA uptake and oxidation by AMPK and ERK1/2 is intensity dependent in rodent muscle.

机译：啮齿动物肌肉中AMPK和ERK1 / 2对收缩诱导的FA摄取和氧化的调节与强度有关。

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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 (R(2) = 0.55, P < 0.05) and between FA oxidation and ERK1/2 phosphorylation from R to E2 (R(2) = 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 (R(2) = 0.04 and R(2) = 0.03, P > 0.05). A positive correlation was also found between FA uptake and FA oxidation and AMPK activity for all exercise intensities (R(2) = 0.57, R(2) = 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.
机译：肌肉收缩激活AMP激活的蛋白激酶（AMPK）和细胞外信号调节激酶（ERK1 / 2），这两个信号分子参与肌肉代谢的调节。这项研究的目的是确定AMPK和/或ERK1 / 2的激活是否有助于调节收缩肌中肌肉脂肪酸（FA）的摄取和氧化。通过操纵火车持续时间（E1 = 25 ms，E2 = 50 ms，E3 = 100 ms，E4 = 200 ms），在强度增加的休息（R）或电刺激（E）期间对大鼠后肢进行灌注。对于匹配的FA递送，在E1，E2和E3期间，FA摄取显着大于R（7.8 +/- 0.7与14.4 +/- 0.3、16.9 +/- 0.8、15.2 +/- 0.5 nmol.min（-1 ）.g（-1），分别为P <0.05），但在E4期间则没有（8.3 +/- 0.3 nmol.min（-1）.g（-1），P> 0.05）。在E1和E2期间，FA氧化显着大于R（1.5 +/- 0.1 vs. 2.3 +/- 0.2，2.5 +/- 0.2 nmol.min（-1）.g（-1），P <0.05）到E3和E4的静止水平（1.8 +/- 0.1和1.5 +/- 0.2 nmol.min（-1）.g（-1），P> 0.05）。发现从R到E3的FA摄取与ERK1 / 2磷酸化之间存在正相关（R（2）= 0.55，P <0.05），从R到E2的FA氧化与ERK1 / 2磷酸化之间（R（2）= 0.76， P <0.05），当分析中分别包含E4和E3和E4的数据时未保持的相关性（R（2）= 0.04和R（2）= 0.03，P> 0.05）。在所有运动强度下，FA摄取与FA氧化和AMPK活性之间也存在正相关（R（2）= 0.57，R（2）= 0.65，P <0.05）。这些结果与我们实验室的先前数据相结合，表明ERK1 / 2和AMPK是分别在中低强度肌肉收缩和中至高强度肌肉收缩期间调节FA摄取和氧化的主要信号分子。 。

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