Regulation of yak longissimus lumborum energy metabolism and tenderness by the AMPK/SIRT1 signaling pathways during postmortem storage

AMPK can activate nicotinamide phosphoribosyltransferase (NAMPT), increasing the ratio of oxidized nicotinamide adenine dinucleotide (NAD(+))/reduced nicotinamide adenine dinucleotide (NADH) ratio, leading to the activation of the energy receptor SIRT1. This pathway is known as the AMPK/SIRT1 signaling pathway. SIRT1 deacetylates and activate LKB1, which is activated by phosphorylation of AMPK (Thr172) and inhibited by phosphorylase-mediated dephosphorylation of AMPK. At the same time, increased AMP/ATP and NAD(+)/NADH ratios lead to the activation of AMPK and SIRT1. SIRT1 and AMPK can activate each other forming a positive feedback loop, which can strengthen catabolism and weaken anabolism thus maintaining energy homeostasis of energy metabolism. At present, there has been no systematic study on AMPK-associated signaling cascades in stored yak meat and details of the AMPK/SIRT1 signaling under these conditions are not known. In this study, NAD(+), NADH were added to yak longissimus thoracic muscles to study AMPK pathway regulation by AMPK/SIRT1 signaling. NAD(+) significantly increased the activity of AMPK and glycolysis during postmortem maturation, increased the rate of energy metabolism, and increased the expression of AMPK protein, indicating that NAD(+) increased energy metabolism in the stored muscle by promoting AMPK activity. NADH treatment inhibited both AMPK activation and glycolysis, together with increasing the pH in the muscle. The results showed that SIRT1 activation elevated the activity of AMPK, leading to its phosphorylation and the activation of glycolysis. Thus, AMPK activity was found to increase in yak meat as an adaptation to hypoxic conditions. This allows more effective regulation of energy production and improves the tenderness of the meat.