Wilson Disease is an autosomal recessive disease resulting in abnormal levels of copper accumulated in the brain, liver, and other vital organs. Metabolomic pathways affected in Wilson Disease are not entirely defined, nor is copper’s effect on zinc homeostasis. This research aims to test the hypothesis that high levels of copper disrupt zinc-dependent processes. In order to interrogate these pathways in Wilson Disease, we analyzed the impact of Wilson Disease treatments, copper chelation therapy, and zinc supplementation on liver and blood metabolites. Liver metabolites were extracted and analyzed via 400 MHZ NMR Spectroscopy and blood serum from experimental groups with Orbitrap-MS and ICP-MS analysis. Preliminary results find that selected liver polar metabolite concentrations were altered by either copper chelation or zinc supplementation in the Wilson’s Disease model and control mice.

Metabolomics analysis of zinc-dependent processes in the Atp7b-/- Wilson disease mouse model

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