Robert S. Britton

TL;DR: The normal relationship between body iron stores and liver hepcidin mRNA levels is altered in Hfe knockout mice, such that liver hePCidin expression is relatively decreased, which is speculated to contribute to the iron homeostasis abnormalities characteristic of HH.

TL;DR: The hypothesis that HFE-/- mice have increased duodenal expression of the divalent metal transporter (DMT1) is tested and support the model for HH in which HFE mutations lead to inappropriately low crypt cell iron, with resultant stabilization of DMT1(IRE) mRNA, up-regulation of DFT, and increased absorption of dietary iron.

TL;DR: It is confirmed that the important role for TFR2 in iron homeostasis is confirmed and provides a tool for investigating the excess iron absorption and abnormal iron distribution in iron-overload disorders.

TL;DR: It is shown that the HLA-H protein not only varies in its pattern of expression along the cranial/caudal axis of the gastrointestinal tract but that it has a unique subcellular localization in the crypts of the small intestine in proximity to the presumed sites of iron absorption.

TL;DR: Although phlebotomy therapy is effective in removing excess iron in hereditary hemochromatosis, chelation therapy is required in the treatment of many patients who have combined secondary and transfusional iron overload due to disorders in erythropoiesis, and deferoxamine treatment has been shown to be effective in preventing iron-induced tissue injury and in prolonging life expectancy.