Authors:

Jennifer Dang

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Wilson's Disease (WD) is characterized by multi-organ copper accumulation due to mutations in the ATP7B gene. The clinical presentations for WD are diverse and sex-based, with females showing hepatic symptoms and males showing neurological symptoms. The pathology of WD is contextualized by the toxicity of copper overload, which promotes oxidative stress and cell death. As a significant site of copper utilization in the cell, mitochondria are targets of copper overload-related toxicity. Thus, their dynamic alterations and fission/fusion activity indicate disease severity. Current WD treatments act as copper chelators but have accessibility and side effect limitations. Metformin, a standard antidiabetic drug, may improve mitochondrial function by chelating copper. Therefore, we aimed to investigate metformin's effects on hepatocellular mitochondrial dynamics in WD mouse models. We treated 18 ATP7B-/- mice with and without metformin for 2 weeks before obtaining liver biopsies for transmission electron microscopy (TEM). Quantitative TEM analysis revealed that in the control group, females exhibited more fission and fusion events than males. However, both sexes showed increased fission and fusion in the treatment group, with females demonstrating more fusion than males. These findings suggest that metformin enhances mitochondrial dynamics and promotes mitochondrial repair in WD in a sex-dependent manner. Discipline Disparities: Examining the Disproportionate Punishment of Black Students in K-12 Schools  Naomi Danner

Source:

UC Davis / VM: Molecular Bio Sciences / 2025

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Co-authors:

Jennifer Dang