Hepatocyte divalent metal-ion transporter-1 is dispensable for hepatic iron accumulation and non-transferrin-bound iron uptake in mice.

摘要: Divalent metal-ion transporter-1 (DMT1) is required for iron uptake by the intestine and developing erythroid cells. DMT1 also present in liver, where it has been implicated of transferrin-bound (TBI) non-transferrin-bound (NTBI), which appears plasma during overload. To test hypothesis that hepatic uptake, we examined mice with Dmt1 gene selectively inactivated hepatocytes (Dmt1liv/liv). We found Dmt1liv/liv controls (Dmt1flox/flox) did not differ terms concentrations or other parameters status. determine if hepatocyte accumulation, crossed Hfe−/− hypotransferrinemic (Trfhpx/hpx) develop Double-mutant Hfe−/−;Dmt1liv/liv Trfhpx/hpx;Dmt1liv/liv were to accumulate similar amounts as their respective controls. directly assess role NTBI TBI injected 59Fe-labeled ferric citrate (for NTBI) 59Fe-transferrin into Dmt1flox/flox measured 59Fe liver. displayed no impairment but was 40% lower. Hepatic levels transferrin receptors 1 2 ZIP14 (ZRT/IRT-like protein 14), may participate unaffected mice. Additionally, liver fed an iron-deficient diet. Conclusion Hepatocyte dispensable accumulation uptake. Although partially mice, suggesting this pathway a minor contributor economy