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1 Department of Animal Science University of Wyoming, Laramie, 82071
* To whom correspondence should be addressed. E-mail: mindu{at}uwyo.edu.
| Abstract |
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Presence of halothane gene results in PSE meat. However, exact mechanisms linking halothane gene and incidence of PSE meat remain unclear. We hypothesize that the presence of halothane gene accelerates energy consumption in postmortem muscle which activates AMP-activated protein kinase (AMPK), leading to enhanced glycolysis and PSE meat. To test our hypothesis, energy status, AMPK activity and glycolysis in the postmortem longissimus dorsi (LD) muscle of halothane gene carrier and halothane negative pigs were compared. Results showed that the presence of halothane gene accelerated energy depletion in postmortem muscle immediately following exsanguination, leading to rapid and early depletion of ATP as shown by an increase in [AMP+IMP]/ATP ratio in postmortem muscle. In addition, an early AMPK activation was observed in LD muscle from halothane carriers. Fructose-2, 6-diphosphate concentration in postmortem muscle was well correlated with AMPK activation. To be a potent stimulator of phosphofructose kinase, the increase in fructose-2, 6-diphosphate is expected to activate phosphofructose kinase, a key enzyme controlling glycolysis, leading to enhanced glycolysis and early accumulation of lactic acid. In summary, this study showed that the presence of halothane gene induced early energy depletion which should be a primary reason causing AMPK activation, leading to accelerated glycolysis and increased incidence of PSE meat. However, AMPK might also be activated by other mechanisms besides energy depletion which warrants further studies.
Key Words: Pigs, halothane gene, AMPK, postmortem, glycolysis, PSE
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