Caffeic acid phenethyl ester ameliorates high-fat diet-induced muscle textural deterioration in grass carp (Ctenopharyngodon idellus) by modulating adipose-muscle crosstalk via myostatin-taz signaling.

The rapid development of aquaculture faces significant challenges, particularly escalating fishmeal costs. Although increasing dietary fat content can partially offset this issue, long-term high-fat diet (HFD) feeding compromises aquatic product quality by deteriorating muscle texture. Previous research demonstrated that shifting adipose tissue expansion toward hyperplasia (rather than hypertrophy) enhances fish tolerance to HFD, but its impact on muscle quality remained unclear. Here, this study investigated how caffeic acid phenethyl ester (CAPE) ameliorates HFD-induced muscle quality deterioration in grass carp (Ctenopharyngodon idellus). A total of 270 fish (initial weight: 360.23 ± 2.07 g) were distributed into 15 cages. Five diets were assigned to triplicate cages for 8 weeks: control (5% lipid, Con), HFD (10% lipid), and HFD + CAPE (400, 800, or 1200 mg/kg) (54 fish per treatment, three cages of 18 fish). The results revealed that CAPE promoted adipocyte hyperplasia by upregulating the relative mRNA expression level of pparγ (P < 0.001) and reducing adipocyte area (P < 0.001), suppressed visceral fat deposition by decreasing the intraperitoneal fat index (P < 0.001), and alleviated adipocyte hypertrophy. Consequently, CAPE significantly improved growth performance by increasing the final body weight (P < 0.001), weight gain rate (P < 0.001), and specific growth rate (P < 0.001), as well as decreasing the feed conversion ratio (P < 0.001). Notably, CAPE did not directly affect myocyte proliferation or differentiation, but significantly reduced the relative mRNA expression of the mstn in adipose tissue (P = 0.001) by modulating adipose expansion patterns through promoted hyperplasia and suppressed hypertrophy. This alleviated Mstn-mediated inhibition of muscular Taz/Hippo signaling pathway, enhancing myocyte differentiation and improving texture parameters (chewiness, hardness, and springiness) in raw/cooked meat (P < 0.05). Present study identified Mstn in fish adipose tissue as a key adipokine mediating adipose-muscle crosstalk: excessive adipocyte hypertrophy impairs muscle quality through Mstn-mediated suppression of muscular Taz/Hippo signaling pathway. These findings elucidate a novel mechanism whereby HFD impairs fish muscle quality by altering adipose tissue expansion patterns, which subsequently modulates its secretory function, thereby confirming the existence of an "adipose-muscle axis", and provide a theoretical foundation for developing functional feed additives targeting adipose expansion modes to mitigate HFD-induced muscle quality deterioration in aquaculture.