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.

该研究的目的是评估膳食亮氨酸对少年金golden鱼T. ovatus胰岛素信号传导途径，葡萄糖代谢和脂肪生成的影响。。总共给300只幼年金po鱼（9.15±0.04 g）喂食了四个等氮日粮，这些日粮中的亮氨酸含量分别为（1.25％，2.77％，5.84和8.73％），分级为8周。将它们随机分配到12个网箱（1.0 m×1.0 m×1.5 m；每个处理三个网箱）中，每个网箱的放养率为25鱼。结果表明，与1.25％（对照组）相比，2.77％的膳食亮氨酸上调了IRS-1，PI3K，AKT和TOR的相对表达，而8.73％的膳食亮氨酸降低了IRS-1的相对表达。与1.25％（对照组）相比，5.84％和8.73％的饮食亮氨酸显着上调了S6K1的相对表达。与1.25％（对照组）相比，2.77％的饮食亮氨酸导致GK，PK，GS和GLUT2的表达水平以及血浆胰岛素水平的增加，而导致PEPCK的抑制。与1.25％（对照组）相比，8.73％的饮食亮氨酸显着降低PK和GLUT2的相对表达以及血浆胰岛素水平，同时增加G6Pase和PEPCK的相对表达以及血糖水平。与1.25％（对照组）相比，2.77％的饮食亮氨酸显着上调了G6PDH，FAS，ACC SREBP1，血浆甘油三酯的相对表达。此外，饮食中的亮氨酸含量为8.73％，导致血浆甘油三酯含量较低。我们的结果表明，PI3K / AKT / TOR胰岛素信号通路介导慢性亮氨酸补充诱导的少年肝糖代谢和脂肪生成 血浆葡萄糖水平。与1.25％（对照组）相比，2.77％的膳食亮氨酸显着上调了G6PDH，FAS，ACC SREBP1，血浆甘油三酯水平的相对表达。此外，饮食中的亮氨酸含量为8.73％，导致血浆甘油三酯含量较低。我们的结果表明，PI3K / AKT / TOR胰岛素信号通路介导慢性亮氨酸补充诱导的少年肝糖代谢和脂肪生成 血浆葡萄糖水平。与1.25％（对照组）相比，2.77％的饮食亮氨酸显着上调了G6PDH，FAS，ACC SREBP1，血浆甘油三酯的相对表达。此外，饮食中的亮氨酸含量为8.73％，导致血浆甘油三酯含量较低。我们的研究结果表明，PI3K / AKT / TOR胰岛素信号通路介导慢性亮氨酸补充诱导的青少年肝糖代谢和脂肪形成卵形山毛榉 最佳水平的亮氨酸可以激活胰岛素信号通路，从而增强卵圆线虫的糖酵解和脂肪酸合成，而饮食中过量的亮氨酸则通过减少胰岛素信号通路和改善糖异生而导致高甘油血症。