Triploid Pacific abalone ( Haliotis discus hannai ) displays pronounced growth superiority and sterility compared with diploids, yet the systemic regulatory mechanisms remain poorly integrated. In this study, we combined transcriptomic and metabolomic analyses to reveal that triploids undergo extensive metabolic reprogramming, leading to a 68.10% increase in foot muscle weight, along with significant improvements in Foot Muscle-Soft Tissue Index and Fullness Index. Multi-omics integration identified four key enriched pathways, with glycolysis and the TCA cycle being the most prominent. Consistent with the omics data, triploids showed elevated levels of glycolytic and TCA intermediates, accompanied by upregulation of rate-limiting enzymes in both pathways. Further mechanistic investigation uncovered that the insulin pathway acts as a central switch activating glucose uptake—mainly through the CAP/Cbl/GLUT4 axis—and enhancing downstream MAPK signaling to promote growth. In parallel, TGF-β signaling contributes to muscle development via a "dual regulation" mode, suppressing the myogenesis inhibitor MSTN while inducing the differentiation promoter BMP7 . These findings provide a comprehensive view of how triploid abalone coordinate energy metabolism and growth regulation, offering novel insights into polyploidy-associated vigor and supporting molecular breeding strategies in aquaculture. • First multi-omics evidence reveals extensive metabolic reprogramming underpins triploid abalone growth superiority. • The insulin pathway centralizes energy regulation via CAP/Cbl/GLUT4 axis, enhancing glucose uptake and MAPK-driven growth. • A novel TGF-β dual-regulation mechanism promotes muscle growth by suppressing MSTN and inducing BMP7.
Zhang et al. (Thu,) studied this question.