Qingwu W. Shen

Pre-slaughter transport, AMP-activated protein kinase, glycolysis, and quality of pork loin.

Numerous studies have revealed that pre-slaughter stress, like transport, increases the occurrence of pale, soft, and exudative (PSE) pork meat. The molecular mechanism underlying this phenomenon, however, is poorly defined. In this study, we investigated the effects of pre-slaughter transport and subsequent rest on energy metabolism, AMP-activated protein kinase (AMPK) activation, and glycolysis in postmortem pork loin. Results indicated that pre-slaughter transport accelerated ATP depletion, which led to lower energy status in postmortem muscle immediately post-exsanguination when compared with control. The lower energy status led to AMPK activation within 1h postmortem, subsequently increasing glycolysis, leading to rapid glycolysis and high incidence of PSE meat. Allowing pigs to rest after transport restored energy status in muscle ante-mortem. Higher energy status then prevented premature and rapid AMPK activation in postmortem muscle and lessened the negative effects of pre-slaughter transport on meat quality. AMPK regulated glycolysis in postmortem muscle, at least partially, through phosphorylation and activation of phosphofructose kinase-2, since fructose-2,6-diphosphate content, an allosteric activator of phosphofructose kinase-1, was well correlated with AMPK activation and glycolytic rate. This suggests that AMPK is a potential molecular target for the control of PSE incidence in pork.

Effects of dietary α-lipoic acid on glycolysis of postmortem muscle

The effects of dietary α-lipoic acid (α-LA) on the pH value, AMP-activated protein kinase (AMPK) activation, and the activities of glycogen phosphorylase and pyruvate kinase in postmortem muscle were investigated. Eighteen C57BL/6J mice were fed diets containing 0%, 0.5%, and 1.0% α-LA. At the end of 2-week feeding trial, the mice were killed and longissimus muscles were sampled at 0-, 1-, and 24-h postmortem for pH determination and enzyme assay. The results showed that dietary α-LA treatment significantly slowed down the decrease of pH values in postmortem muscle. The ultimate pH values in postmortem muscle of mice receiving 0.5% and 1.0% α-LA treatments were 6.40 and 6.63, respectively, significantly higher than that (6.21) of no α-LA treatment (p<0.05). AMPK was activated at the early postmortem stage. Dietary α-LA can suppress the activation of AMPK in postmortem muscle. At 1- and 24-h postmortem, activities of AMPK were much lower in postmortem muscle of mice receiving 0.5% and 1.0% α-LA treatments than that with no α-LA treatment. Between these two dietary α-LA treatments, however, no difference in AMPK activity was observed, indicating that 0.5% dietary α-LA is enough to suppress AMPK in postmortem muscle. Similar to AMPK, glycogen phosphorylase activity was higher in the treatment without dietary α-LA than those with 0.5% and 1.0% dietary α-LA supplements. No difference in the activity of glycogen phosphorylase was observed between the 0.5% and 1.0% dietary α-LA treatments. Dietary α-LA had no significant influence on the activity of pyruvate kinase in postmortem muscle. All these results indicate that AMPK plays a role in glycolysis in postmortem muscle. Dietary α-LA supplementation can suppress the activation of AMPK in postmortem muscle, down-regulate the activity of glycogen phosphorylase, resulting in a higher ultimate pH values in postmortem muscle. Therefore, dietary α-LA supplementation is a potential way to reduce the incidence of pale, soft, exudative (PSE) meat.