Wuxi Fisheries College, Nanjing Agricultural University, Wuxi, 214081, China.
Division of Aquaculture, College of Agriculture, Food Science and Sustainable Systems (CAFSSS), Kentucky State University, 103 Athletic Road, Frankfort, KY, 40601, USA.
Sci Rep. 2017 Aug 11;7(1):7864. doi: 10.1038/s41598-017-06104-3.
This study evaluated the mechanisms governing insulin resistance, glucose metabolism and lipogenesis in juvenile fish fed with graded levels of dietary arginine. The results showed that, compared with the control group (0.87%), 2.31% dietary arginine level resulted in the upregulation of the relative gene expression of IRS-1, PI3K and Akt in the insulin signaling pathway, while 2.70% dietary arginine level led to inhibition of these genes. 1.62% dietary arginine level upregulated glycolysis by increasing GK mRNA level; 2.70% dietary arginine level upregulated gluconeogenesis and resulted in high plasma glucose content by increasing PEPCK and G6P mRNA level. Furthermore, 2.70% dietary arginine level significantly lowered GLUT2 and increased PK mRNA levels. 1.62% dietary arginine level significantly upregulated ACC, FAS and G6PDH mRNA levels in the fat synthesis pathway and resulted in high plasma TG content. These results indicate that 1.62% dietary arginine level improves glycolysis and fatty acid synthesis in juvenile blunt snout bream. However, 2.70% dietary arginine level results in high plasma glucose, which could lead to negative feedback of insulin resistance, including inhibition of IRS-1 mRNA levels and activation of gluconeogenesis-related gene expression. This mechanism seems to be different from mammals at the molecular level.
本研究评估了在不同水平的日粮精氨酸条件下,控制幼鱼胰岛素抵抗、糖代谢和脂肪生成的机制。结果表明,与对照组(0.87%)相比,2.31%日粮精氨酸水平上调了胰岛素信号通路中 IRS-1、PI3K 和 Akt 的相对基因表达,而 2.70%日粮精氨酸水平则抑制了这些基因的表达。1.62%日粮精氨酸水平通过增加 GK mRNA 水平促进糖酵解;2.70%日粮精氨酸水平通过增加 PEPCK 和 G6P mRNA 水平促进糖异生,导致高血糖含量。此外,2.70%日粮精氨酸水平显著降低 GLUT2 和增加 PK mRNA 水平。1.62%日粮精氨酸水平显著上调脂肪合成途径中 ACC、FAS 和 G6PDH mRNA 水平,导致高血糖 TG 含量。这些结果表明,1.62%日粮精氨酸水平可改善幼钝吻鲷的糖酵解和脂肪酸合成。然而,2.70%日粮精氨酸水平导致高血糖,可能导致胰岛素抵抗的负反馈,包括 IRS-1 mRNA 水平的抑制和糖异生相关基因表达的激活。这种机制在分子水平上似乎与哺乳动物不同。