The differences in muscle development potential between male and female ducks lead to variations in body weight, significantly affecting the growth of the Muscovy duck meat industry. The aim of this study is to explore the regulatory mechanisms for the muscle development differences between genders. Muscovy ducks of both sexes were selected for measurements of body weight, growth traits, hormone levels, and muscle gene expression. The results show that male ducks compared to females had greater weight and growth traits (p < 0.05). Compared to male ducks, the level of serum testosterone in female ducks was decreased, and the estradiol levels were increased (p < 0.05). The RNA-seq analysis identified 102 upregulated and 49 downregulated differentially expressed genes. KEGG analysis revealed that among the top 10 differentially enriched pathways, the AMPK signaling pathway is closely related to muscle growth and development. Additionally, the mRNA and protein levels of CD36, CPT1A, LPL, and SREBP1 were increased and the P-AMPK protein level decreased in the female ducks compared to the male ducks (p < 0.05). In conclusion, muscle development potential difference between male and female ducks is regulated by sex hormones. This process is likely mediated through the activation of the AMPK pathway.

Viruses have evolved numerous mechanisms to target key metabolic pathways in the host, thereby reshaping host metabolism to establish a metabolic environment conducive to their replication. We previously observed that pseudorabies virus (PRV) infection upregulates cellular glycolysis, but the mechanism is not clear. Here, our results showed that PRV infection significantly upregulated the mRNA levels of HK2 and MCT4. Upon HIF-1α inhibition, the PRV-induced upregulation of glycolytic genes was reversed. Concurrently, PRV infection promoted the accumulation of intracellular mitochondrial ROS (mROS), whereas mROS inhibition blocked HIF-1α activation. Furthermore, both HIF-1α and mROS inhibition significantly reduced PRV replication. In conclusion, we revealed that PRV activates HIF-1α by inducing mROS accumulation, thereby upregulating key glycolytic genes to promote viral replication. This study provides novel evidence for the metabolic regulatory mechanisms underlying PRV infection and identifies potential targets for PRV and other herpesvirus control.