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Skeletal muscle is the largest metabolic organ in the body, and its metabolic flexibility is essential for maintaining systemic energy homeostasis. Metabolic inflexibility in muscles is a dominant cause of various metabolic disorders, impeding muscle development. In our previous study, we found lncRNA  ZFP36L2-AS  (for “ ZFP36L2 -antisense transcript”) is specifically enriched in skeletal muscle. Here, we report that  ZFP36L2-AS  is upregulated during myogenic differentiation, and highly expressed in breast and leg muscle. In vitro,  ZFP36L2-AS  inhibits myoblast proliferation but promotes myoblast differentiation. In vivo,  ZFP36L2-AS  facilitates intramuscular fat deposition, as well as activates fast-twitch muscle phenotype and induces muscle atrophy. Mechanistically,  ZFP36L2-AS  interacts with acetyl-CoA carboxylase alpha (ACACA) and pyruvate carboxylase (PC) to induce ACACA dephosphorylation and damaged PC protein stability, thus modulating muscle metabolism. Meanwhile,  ZFP36L2-AS  can activate ACACA to reduce acetyl-CoA content, which enhances the inhibition of PC activity. Our findings present a novel model about the regulation of lncRNA on muscle metabolism.

Long noncoding RNA ZFP36L2-AS functions as a metabolic modulator to regulate muscle development