Study of the AMP-Activated Protein Kinase Role in Energy Metabolism Changes during the Postmortem Aging of Yak Longissimus dorsal.

Abstract

Simple SummaryPale, 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.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.