Fig. 7

A schematic diagram for the regulatory mechanism of Se in skeletal muscle fibre hypertrophy in zebrafish. (a) Under Se adequate status, zebrafish skeletal muscle exhibits a low concentration of ROS, an active PI3K-Akt-TORC1 signalling and an efficient protein synthesis, which attribute to maintain the normal hypertrophy process of skeletal muscle fibres in zebrafish. (b) Under Se-deficient status, the down-regulation of antioxidant selenoproteins lead to a high concentration of ROS. The high concentration of ROS dephosphorylates and inactivate Akt, thereby inhibiting TORC1 pathway-mediated protein synthesis and leading to the suppressed hypertrophy of skeletal muscle fibres. IGF1, insulin-like growth factor 1; IRSs, insulin receptor substrates; PI3K, phosphatidylinositol-3-kinase; PIP2, phosphoinositide-4,5-biphosphate; PIP3, phosphoinositide-3,4,5-triphosphate; PDK1, phosphoinositide-dependent kinase 1; Akt, protein kinase B; TORC1, the target of rapamycin complex 1; TORC2, the target of rapamycin complex 2; ROS, reactive oxygen species.