To investigate the effect of chromium and iron on glucose metabolism via the PI3K/Akt/GLUT4 signaling pathway. Skeletal muscle gene microarray data in T2DM (GSE7014) was selected using Gene Expression Omnibus database. Element-gene interaction datasets of chromium and iron were extracted from comparative toxicogenomics database (CTD). Gene ontology (GO)and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using DAVID online tool. Cell viability, insulin-stimulated glucose uptake, intracellular reactive oxygen species (ROS) level, and protein expression level were measured in C2C12 cells. The bioinformatics research indicated that PI3K/Akt signaling pathway participated in the effects of chromium and iron associated with T2DM. Insulin-stimulated glucose uptake level was significantly higher in chromium picolinate (Cr group) and lower in ammonium iron citrate (FA group) than that for the control group (P < 0.05); chromium picolinate + ammonium iron citrate (Cr + FA group) glucose uptake level was higher than that for the FA group (P < 0.05). Intracellular ROS level was significantly higher in the FAC group than that for the control group (P < 0.05), and that for the Cr + FA group was lower than that for the FA group (P < 0.05). p-PI3K/PI3K, p-Akt/Akt, and GLUT4 levels were significantly lower in the FA group than that for the control group (P < 0.05), and the Cr + FA group had higher levels than the FA group (P < 0.05). Chromium might have a protective effect on iron-induced glucose metabolism abnormalities through the ROS-mediated PI3K/Akt/GLUT4 signaling pathway.

研究铬和铁通过 PI3K/Akt/GLUT4 信号通路对葡萄糖代谢的影响。使用基因表达综合数据库选择 T2DM (GSE7014) 中的骨骼肌基因微阵列数据。铬和铁的元素-基因相互作用数据集是从比较毒物基因组数据库（CTD）中提取的。使用DAVID在线工具进行基因本体论（GO）和京都基因和基因组百科全书（KEGG）富集分析。测量 C2C12细胞的细胞活力、胰岛素刺激的葡萄糖摄取、细胞内活性氧 (ROS) 水平和蛋白质表达水平。生物信息学研究表明PI3K/Akt信号通路参与了铬、铁与T2DM相关的作用。吡啶甲酸铬组（Cr组）胰岛素刺激葡萄糖摄取水平显着高于对照组（P < 0.05），柠檬酸铁铵组（FA组）则低于对照组（ P < 0.05）；吡啶甲酸铬+柠檬酸铁铵（Cr+FA组）葡萄糖摄取水平高于FA组（ P < 0.05）。 FAC 组细胞内 ROS 水平显着高于对照组（ P < 0.05），Cr+FA 组细胞内 ROS 水平低于 FA 组（ P < 0.05）。 FA 组 p-PI3K/PI3K、p-Akt/Akt、GLUT4 水平显着低于对照组（ P < 0.05），且 Cr+FA 组高于 FA 组（ P < 0.05）。 0.05）。铬可能通过 ROS 介导的 PI3K/Akt/GLUT4 信号通路对铁诱导的葡萄糖代谢异常具有保护作用。