Methionine deficiency affects myogenesis and muscle macronutrient metabolism in juvenile turbot Scophthalmus maximus

The study was aimed to explore the impacts of dietary methionine availability on muscle growth and macronutrient metabolism in turbot. Based the optimal dietary methionine requirement, three isonitrogenous and isolipidic diets with different methionine levels (0.91%, 1.90%, and 2.90%) were formulated. 270 fish (average weight 7.40 +/- 0.01 g) were distributed into 9 fiberglass tanks and fed for 10 weeks. Results showed that methionine deprivation significantly depressed fish growth and reduced the crude protein content in the whole body and muscle. Methionine deprivation inhibited the expression of myogenic differentiation antigen D (myoD), myogenin and myosin light chain (mlc) while induced myostatin expression. Methionine deficiency inhibited the mechanistic target of rapamycin (mTOR) pathway and activated the autophagy-lysosomal and ubiquitin-proteasome systems. The AMP-activated protein kinase (AMPK) was activated and uncoupling protein 1 (ucp1) was up-regulated when dietary methionine was deficient. Meanwhile, methionine deficiency reduced total free amino acid content, promoted the catabolism of amino acid, and improved the flux of tricarboxylic acid cycle (acetyl-CoA, fumarate, malate, and oxoglutarate). Methionine deficiency depressed the glycolysis and lipogenesis processes, while elevated fatty acid beta-oxidation, which shifted the fuel utilization in muscle. Excess methionine intake did not further modulate the cell signaling and metabolism in muscle. Our results provide new clues on the involvement of dietary methionine on muscle growth and metabolic responses in teleost.