{Reference Type}: Journal Article
{Title}: A comparative study of urinary levels of multiple metals and neurotransmitter correlations between GDM and T2DM populations.
{Author}: Yu J;Wang C;Liu Y;Tao T;Yang L;Liu R;Liang D;Zhang Y;He Z;Sun Y;
{Journal}: J Trace Elem Med Biol
{Volume}: 84
{Issue}: 0
{Year}: 2024 Jul 8
{Factor}: 3.995
{DOI}: 10.1016/j.jtemb.2024.127447
{Abstract}: <B>OBJECTIVE: </B>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.<BR><B>METHODS: </B>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.<BR><B>RESULTS: </B>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.<BR><B>CONCLUSIONS: </B>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.