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Mice Lacking β‐catenin In Liver Develop Hepatic Fibrosis In Response To Iron Overload

Dysregulated Wnt/β‐catenin signaling and iron overload disorders like hemochromatosis have been implicated in hepatocellular carcinoma. We sought to identify a potential link between Wnt/β‐catenin signaling and hepatic iron metabolism by subjecting mice to an iron‐overload diet. Hepatocyte‐specific β‐catenin knockout (KO) and littermate control (CON) mice were subjected to a 10,000 ppm iron diet for three months. Mice on the iron diet showed larger liver weight to body weight ratios than their counterparts on the control diet, which was accompanied by an increase in proliferation. Steatosis was observed in all groups after iron, corresponding to an increase in triglycerides and cholesterol esters. Interestingly, KO mice after iron diet had notably more fibrosis and inflammation compared to CON. In addition, a greater number of macrophages containing iron‐laden hepatocytes were evident in KO. Taken together, these results suggest β‐catenin‐deficient mice are more prone to injury, inflammation, and fibrosis in response to iron overload. Thus, this may be a useful model to study human hemochromatosis since most mouse models exposed to high iron do not exhibit hepatic fibrosis.