AMPK-mediated energy metabolism disorders are associated with impaired type IIB muscle fiber regeneration in broiler chickens with wooden breast myopathy.

Abstract

Wooden breast (WB) myopathy is a myodegenerative muscle disease, in which muscle regeneration is also commonly observed, and has been increasingly reported in fast-growing broilers in recent years. This study aims to investigate the underlying mechanism of energy metabolism abnormalities on muscle regeneration in WB. A total of 300 male Ross 308 broilers were evaluated at 42 days of age based on physical and biochemical examinations to classify the severity of WB. From these, 16 broilers were selected for each of three groups: the normal group (CON), the moderate WB group (WB-M), and the severe WB group (WB-S). Compared to CON, WB were heavier, thicker, harder and had lower meat quality. Additionally, WB exhibited disturbance of energy metabolism, with increased cholesterol and triglycerides and decreased glycogen and lactate contents. Meanwhile, WB exhibited muscle regeneration as illustrated by the increased central nuclei and inflammation cells in muscle and higher creatine kinase activity in serum and muscle. WB exhibited inhibition of AMPK activity, with lower phosphorylation at Thr172 and higher phosphorylation at Ser496. Consistently, WB dysregulated the downstream pathways of AMPK, such as protein synthesis activity, glycolysis activity, lipid metabolism activity, and inflammatory response. Furthermore, in primary myoblasts, AMPK activation suppressed type II B myofiber hypertrophy, while its inhibition enhanced hypertrophy. In conclusion, this study provides evidence that abnormal ⅡB myofiber regeneration associated with imbalance in AMPK-mediated energy homeostasis, plays a crucial role in the pathogenesis of WB. These finding may provide new insights into mitigating the onset of WB.