Effects of dietary leucine on glucose metabolism, lipogenesis and insulin pathway in juvenile golden pompano Trachinotus ovatus

Abstract

The aim of the study was to evaluate the effects of dietary leucine on the insulin signaling pathway, glucose metabolism and lipogenesis in juvenile golden pompano T. ovatus. A total of 300 juvenile golden pompano (9.15 ± 0.04 g) were fed four isonitrogenous diets with graded levels of leucine (1.25 %, 2.77 %, 5.84 and 8.73 %) for 8 weeks. They were randomly distributed to 12 cages (1.0 m × 1.0 m × 1.5 m; three cages per treatment) at an equal stocking rate of 25 fish per cage. Results indicated that compared with 1.25 % (the control), 2.77 % dietary leucine upregulated the relative expressions of IRS-1, PI3K, AKT and TOR, while 8.73 % dietary leucine lowered the relative expression of IRS-1. Compared with 1.25 % (the control), 5.84 % and 8.73 % dietary leucine significantly upregulated the relative expression of S6K1. Compared with 1.25 % (the control), 2.77 % dietary leucine led to the increment of the expression levels of GK, PK, GS and GLUT2, and the plasma insulin level, while led to inhibition of PEPCK. Compared with 1.25 % (the control), 8.73 % dietary leucine significantly decreased the relative expressions of PK and GLUT2, and plasma insulin level, while increase the relative expressions of G6Pase and PEPCK, plasma glucose level. Compared with 1.25 % (the control), 2.77 % dietary leucine significantly upregulated the relative expression of G6PDH, FAS, ACC SREBP1, plasma triglyceride level. Furthermore, 8.73 % dietary leucine resulted in low plasma triglyceride content. Our results suggest that the PI3K/AKT/TOR insulin signaling pathway mediates chronic leucine supplementation induced hepatic glucose metabolism and lipogenesis in juvenile T. ovatus. Optimal level of leucine could activate insulin signaling pathway, thus enhance the glycolysis and fatty acid synthesis in juvenile T. ovatus, while dietary excess leucine resulted in hyperglyceria by reducing the insulin signaling pathway and improving gluconeogenesis.