To investigate the effect of iron overload on glucose metabolism and the underlying mechanism, Irp2 knockout (Irp2<sup>-/-</sup>) mice (endogenous iron overload model) were used.
Together with previous data obtained in the presence of iron excess, these results show that the parallel degradation pathways through lysosomes and the proteasome that are active on IRP2 under normal growth conditions are preferentially shifted to the proteasome when iron becomes plentiful.