Study of the AMP-activated Protein Kinase Role in Energy Metabolism Changes during the Postmortem Aging of Yak Longissimus dorsal
Study of the AMP-activated Protein Kinase Role in Energy Metabolism Changes during the Postmortem Aging of Yak Longissimus dorsal
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DOI：
10.3390/ani10030427
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发表时间：
2020-03
期刊：
影响因子：
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通讯作者：
Yayuan Yang;Ling Han;Qunli Yu;Yongfang Gao;Rende Song
中科院分区：
文献类型：
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作者：
Yayuan Yang;Ling Han;Qunli Yu;Yongfang Gao;Rende Song
苍白、柔软和渗出（PSE）肉的特点是苍白、潮湿和海绵状的外观。研究表明，由于死后快速糖酵解引起的早期乳酸积累，加上肌肉温度高，是PSE肉的原因，尽管精确的分子机制仍不清楚。我们假设单磷酸腺苷活化蛋白激酶（AMPK）是调节肉死后糖酵解的关键因子。为此，我们分别使用AICAR和STO-609激活和抑制牦牛肌肉中的AMPK，并分析其代谢参数。本研究的目的是确定AMPK在死后糖酵解中的关键作用，以及以AMPK为靶点以减少糖酵解并将PSE肉的风险降至最低的可能性。牦牛适应较高的海拔和较低的大气含氧量。因此，在低氧适应条件下，牦牛AMPK活性增加，加速糖酵解，优化能量产生。我们使用AMPK抑制剂STO-609和特异性激活剂AICAR进一步研究了AMPK在死后肌糖酵解调节中的作用。本研究的目的是确认AMPK在牦牛死后糖酵解中的关键作用，以及它作为减少糖酵解和研究能量代谢的靶点的潜力。摘要为探讨牦牛死后肌肉的生理机制，本试验研究了单磷酸腺苷活化蛋白激酶（AMPK）的活性及其在牦牛死后能量代谢中的作用。本实验通过注射AMPK特异性激活剂5-氨基-1- β -d-呋喃丙基咪唑-4-甲酰胺（AICAR）和STO-609，观察死后牦牛成熟过程中糖酵解、能量代谢、AMPK活性和AMPK基因（PRKA1和PRKA2）表达的变化。结果表明，AICAR可增加PRKKA1和PRKAA2基因的表达，激活AMPK，提高其活性。AICAR的作用包括降低ATP浓度，增加AMP的产生，加速糖酵解，增加乳酸浓度，降低pH值。相比之下，STO-609具有相反的效果。在低氧适应下，肉AMPK活性增加，糖酵解和代谢加速，更有效地调节能量代谢。因此，本研究为建立牦牛死后肉能量代谢理论体系奠定了基础。
Simple Summary Pale, soft, and exudative (PSE) meat is characterized by a pallid, sodden, and spongy appearance. Studies show that an early buildup of lactic acid due to rapid postmortem glycolysis, coupled with high muscle temperature, is the cause of PSE meat, although the precise molecular mechanisms remain poorly defined. We hypothesized that adenosine monophosphate activated protein kinase (AMPK) is the key factor regulating postmortem glycolysis in meat. To this end, we respectively activated and inhibited AMPK in yak muscle using AICAR and STO-609 and analyzed the metabolism parameters. The objective of this study was to establish the crucial role of AMPK in postmortem glycolysis and the possibility of targeting AMPK in order to reduce glycolysis and minimize the risk of PSE meat. Yaks are adapted to higher altitudes and lower atmospheric oxygen levels. Therefore, the activity of the yak AMPK is increased under hypoxic adaptation, which accelerates glycolysis and optimizes energy production. We further investigated the role of AMPK in the regulation of postmortem muscle glycolysis using the AMPK inhibitor STO-609 and specific activator AICAR. The objective of this study was to confirm the crucial role of AMPK in postmortem glycolysis and its potential as a target to reduce glycolysis and study of energy metabolism in yak. Abstract To explore the postmortem physiological mechanism of muscle, activity of adenosine monophosphate activated protein kinase (AMPK) as well as its role in energy metabolism of postmortem yaks were studied. In this experiment, we injected 5-amino-1-beta-d-furanonyl imidazole-4-formamide (AICAR), a specific activator of AMPK, and STO-609 to observe the changes in glycolysis, energy metabolism, AMPK activity, and AMPK gene expression (PRKA1 and PRKA2) in postmortem yaks during maturation. The results showed that AICAR could increase the expression of the PRKKA1 and PRKAA2 genes, activate AMPK and increase its activity. The effects of AICAR include a lower concentration of ATP, an increase in AMP production, an acceleration of glycolysis, an increase in the lactic acid concentration, and a decrease in the pH value. In contrast, STO-609 had the opposite effect. Under hypoxic adaptation, the activity of the meat AMPK increased, which accelerated glycolysis and metabolism and more effectively regulated energy metabolism. Therefore, this study lays the foundation for establishing a theoretical system of energy metabolism in postmortem yak meat.