■在这项研究中,两种压力源的综合作用,即,来自手机和果糖消耗的电磁场(EMFs),阐明了AMPK/SIRT1-UCP2/FOXO1途径的下丘脑和肝脏主要代谢调节因子,以描述胰岛素抵抗的潜在分子机制。
■断奶的Wistar大鼠(28天大)分为4组:正常,仅曝光(ExpO),仅果糖(FruO),和暴露和果糖(EF)。每组免费提供标准实验室食物8周。此外,控制组,即,正常和FruO组,不受限制地获得饮用水和果糖溶液(15%),分别。此外,各自的治疗组,即,ExpO和EF组,接收到的EMF暴露(1,760MHz,2小时/天×8周)。在成年早期,线粒体功能,胰岛素受体信号,使用蛋白质印迹和生化分析评估下丘脑和肝组织中的氧化应激信号。
■在EF的下丘脑组织中,SIRT1,FOXO1,p-PI3K,p-AKT,复杂III,UCP2,MnSOD,过氧化氢酶表达、OXPHOS和GSH活性均较正常组显著降低(P<0.05),ExpO,和FruO组。在EF的肝组织中,p-AMPKα,SIRT1,FOXO1,IRS1,p-PI3K,复杂I,II,III,IV,V,UCP2和MnSOD的表达和OXPHOS的活性,SOD,过氧化氢酶,与正常组相比,GSH明显降低(P<0.05)。
■研究结果表明,在Wistar大鼠的童年和青春期,EMF暴露和果糖消耗的结合破坏了胰岛素受体信号的紧密关联和多重调节的串扰,线粒体OXPHOS,以及下丘脑和肝脏的抗氧化防御系统。
UNASSIGNED: In this study, the combined effect of two stressors, namely, electromagnetic fields (EMFs) from mobile phones and fructose consumption, on hypothalamic and hepatic master metabolic regulators of the AMPK/SIRT1-UCP2/FOXO1 pathway were elucidated to delineate the underlying molecular mechanisms of insulin resistance.
UNASSIGNED: Weaned Wistar rats (28 days old) were divided into 4 groups: Normal, Exposure Only (ExpO), Fructose Only (FruO), and Exposure and Fructose (EF). Each group was provided standard laboratory chow ad libitum for 8 weeks . Additionally, the control groups, namely, the Normal and FruO groups, had unrestricted access to drinking water and fructose solution (15%), respectively. Furthermore, the respective treatment groups, namely, the ExpO and EF groups, received EMF exposure (1,760 MHz, 2 h/day x 8 weeks). In early adulthood, mitochondrial function, insulin receptor signaling, and oxidative stress signals in hypothalamic and hepatic tissues were assessed using western blotting and biochemical analysis.
UNASSIGNED: In the hypothalamic tissue of EF, SIRT1, FOXO 1, p-PI3K, p-AKT, Complex III, UCP2, MnSOD, and catalase expressions and OXPHOS and GSH activities were significantly decreased ( P < 0.05) compared to the Normal, ExpO, and FruO groups. In hepatic tissue of EF, the p-AMPKα, SIRT1, FOXO1, IRS1, p-PI3K, Complex I, II, III, IV, V, UCP2, and MnSOD expressions and the activity of OXPHOS, SOD, catalase, and GSH were significantly reduced compared to the Normal group ( P < 0.05).
UNASSIGNED: The findings suggest that the combination of EMF exposure and fructose consumption during childhood and adolescence in Wistar rats disrupts the closely interlinked and multi-regulated crosstalk of insulin receptor signals, mitochondrial OXPHOS, and the antioxidant defense system in the hypothalamus and liver.