Intracellular Calcium Overload and Activation of CaMKK/AMPK Signaling Are Related to the Acceleration of Muscle Glycolysis of Broiler Chickens Subjected to Acute Stress.

Abstract

The current study investigated the effect of preslaughter transport on stress response and meat quality of broilers and explored the underlying mechanisms involved in the regulation of muscle glycolysis through calcium/calmodulin-dependent protein kinase kinase (CaMKK)/AMP-activated protein kinase (AMPK) signaling. Results suggested that transport induced stress responses of broilers and caused PSE-like syndrome of pectoralis major muscle. Preslaughter transport enhanced the mRNA expressions of glycogen phosphorylase and glucose transporters, as well as the activities of glycolytic enzymes, which accelerated the breakdown of glycolytic substrates and the accumulation of lactic acid. In addition, acute stress induced abnormal intracellular calcium homeostasis by disrupting calcium channels on the cell membrane and sarcoplasmic reticulum, which led to the activation of CaMKK and promoted AMPK phosphorylation. This study provides evidence that the intracellular calcium overload and the enhancement of CaMKK/AMPK signaling are related to the accelerated muscle glycolysis of broiler chickens subjected to acute stress.