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Key Points Most cases of hereditary hemochromatosis (HH) result from mutations in the HFE gene, consequential low hepcidin levels and continued iron absorption from the gut despite high iron levels Homozygosity for the Cys282Tyr HFE gene mutation occurs in 0.30.7% of people with North European ancestry, but clinical disease occurs in only a small percentage of these Pathophysiology of diabetes mellitus in iron overload is thought to be a result of -cell dysfunction that leads to inadequate insulin secretion for the prevailing degree of insulin sensitivity Increased oxidative stress may be one mechanism whereby iron overload causes -cell dysfunction and -cell apoptosis Early identification and treatment with phlebotomy before the onset of diabetes mellitus and cirrhosis can prevent the increased morbidity and mortality associated with HH This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access $189.00 per year only $15.75 per issue Buy this article Purchase on SpringerLink Instant access to the full article PDF

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