Abstract：
OBJECTIVE: The pathogenesis of GDM and T2DM are closely related to various metals in vivo, and changes in the concentration of these metal exposures can lead to neuropathy through the DNA damage pathway caused by the accumulation of ROS.
METHODS: Urine samples were analyzed for heavy metals and trace elements by ICP-MS, neurotransmitter metabolites by HPLC, 8-OH-dG by HPLC-MS and metabolomics by UPLC-MS.
RESULTS: Cd and Hg were risk factors for T2DM. There was a positive correlation between 8-OH-dG and neurotransmitter metabolites in both two populations. For GDM, the metabolite with the largest down-regulation effect was desloratadine and the largest up-regulation effect was D-glycine. That tyrosine and carbon metabolites were upregulated in the GDM population and downregulated in the T2DM population.
CONCLUSIONS: The BMI, urinary Cd and Hg endo-exposure levels correlated with elevated blood glucose, and the latter may cause changes in the DNA damage marker 8-OH-dG in both study populations and trigger common responses to neurological alterations changes in the neurotransmitter. Tyrosine, carbonin metabolites, alanine, aspartate, and glutamate were signature metabolites that were altered in both study populations. These indicators and markers have clinical implications for monitoring and prevention of neurological injury in patients with GDM and T2DM.
METHODS: Urine samples were analyzed for heavy metals and trace elements by ICP-MS, neurotransmitter metabolites by HPLC, 8-OH-dG by HPLC-MS and metabolomics by UPLC-MS.
RESULTS: Cd and Hg were risk factors for T2DM. There was a positive correlation between 8-OH-dG and neurotransmitter metabolites in both two populations. For GDM, the metabolite with the largest down-regulation effect was desloratadine and the largest up-regulation effect was D-glycine. That tyrosine and carbon metabolites were upregulated in the GDM population and downregulated in the T2DM population.
CONCLUSIONS: The BMI, urinary Cd and Hg endo-exposure levels correlated with elevated blood glucose, and the latter may cause changes in the DNA damage marker 8-OH-dG in both study populations and trigger common responses to neurological alterations changes in the neurotransmitter. Tyrosine, carbonin metabolites, alanine, aspartate, and glutamate were signature metabolites that were altered in both study populations. These indicators and markers have clinical implications for monitoring and prevention of neurological injury in patients with GDM and T2DM.
摘要：
目的：GDM和T2DM的发病机制与体内多种金属密切相关。这些金属暴露浓度的变化可通过ROS积累引起的DNA损伤途径导致神经病变。
方法：通过ICP-MS分析尿液样品中的重金属和微量元素，通过HPLC，神经递质代谢产物，8-OH-dG的HPLC-MS和代谢组学的UPLC-MS。
结果：Cd和Hg是T2DM的危险因素。在两个种群中，8-OH-dG与神经递质代谢产物之间均呈正相关。对于GDM，下调作用最大的代谢产物是地氯雷他定,上调作用最大的代谢产物是D-甘氨酸.酪氨酸和碳代谢物在GDM人群中上调，在T2DM人群中下调。
结论：BMI，尿镉和汞体内暴露水平与血糖升高相关，后者可能会导致两个研究人群中DNA损伤标记8-OH-dG的变化，并引发对神经递质神经系统变化的共同反应。酪氨酸,碳素代谢物，丙氨酸,天冬氨酸,和谷氨酸是在两个研究人群中发生改变的特征代谢物。这些指标和标志物对GDM和T2DM患者神经损伤的监测和预防具有临床意义。
方法：通过ICP-MS分析尿液样品中的重金属和微量元素，通过HPLC，神经递质代谢产物，8-OH-dG的HPLC-MS和代谢组学的UPLC-MS。
结果：Cd和Hg是T2DM的危险因素。在两个种群中，8-OH-dG与神经递质代谢产物之间均呈正相关。对于GDM，下调作用最大的代谢产物是地氯雷他定,上调作用最大的代谢产物是D-甘氨酸.酪氨酸和碳代谢物在GDM人群中上调，在T2DM人群中下调。
结论：BMI，尿镉和汞体内暴露水平与血糖升高相关，后者可能会导致两个研究人群中DNA损伤标记8-OH-dG的变化，并引发对神经递质神经系统变化的共同反应。酪氨酸,碳素代谢物，丙氨酸,天冬氨酸,和谷氨酸是在两个研究人群中发生改变的特征代谢物。这些指标和标志物对GDM和T2DM患者神经损伤的监测和预防具有临床意义。
