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Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
Published on: May 10, 2022
Hepatic iron accumulation is reduced in the cholestatic Mdr2-/- mouse
Amy L Sobbe1,2, Kim Bridle1,2, Lesley-Anne Jaskowski1,2
1Faculty of Health, Medicine and Behavioural Sciences, The University of Queensland, Brisbane, Australia.
Bioscience Reports
|July 10, 2026
Summary
The Mdr2-/- mouse model shows abnormal iron regulation in cholestatic liver disease. Despite reduced hepcidin, these mice exhibit impaired iron uptake, leading to lower liver iron stores.
Area of Science:
- Hepatology
- Iron Metabolism
- Cholestasis Research
Background:
- The multidrug-resistance 2 knockout (Mdr2-/-) mouse models biliary liver injury, resembling human progressive familial intrahepatic cholestasis type 3.
- Cholestasis-induced bile acid accumulation is linked to decreased hepcidin, suggesting a connection between liver disease and iron homeostasis.
Purpose of the Study:
- To investigate iron homeostasis in the Mdr2-/- mouse model of cholestasis.
- To analyze iron levels and the expression of iron-related genes in Mdr2-/- mice.
Main Methods:
- Real-time PCR and western blotting were used to analyze iron levels and gene expression.
- Wild-type and Mdr2-/- mice were fed either an iron-deficient or a carbonyl iron diet to assess iron accumulation and hepcidin response.
Main Results:
- Mdr2-/- mice on a control diet had reduced hepatic iron stores despite lower hepcidin expression and higher transferrin receptor 1 expression.
- Mice fed a carbonyl iron diet were resistant to hepatic iron accumulation, indicating impaired hepatocyte iron uptake.
Conclusions:
- Mdr2-/- mice exhibit abnormal hepatic iron homeostasis, likely due to cholestasis.
- Impaired hepatic iron uptake may explain the lower liver iron content observed in cholestatic conditions compared to hepatocellular diseases.
