Iron metabolism and the polycystic ovary syndrome

The polycystic ovary syndrome (PCOS) is associated with insulin resistance and abnormal glucose tolerance. Iron overload may lead also to insulin resistance and diabetes. Serum ferritin levels are increased in PCOS, especially when glucose tolerance is abnormal, suggesting mild iron overload. Factors contributing to potential iron overload in PCOS include the iron sparing effect of chronic menstrual dysfunction, insulin resistance, and a decrease in hepcidin leading to increased iron absorption. Enhancement of erythropoiesis by androgen excess is unlikely, because soluble transferrin receptor levels are not increased in PCOS. Future venues of research should address the long-term effects of PCOS treatment on iron overload and, conversely, the possible effects of iron lowering strategies on the glucose tolerance of patients with PCOS. The polycystic ovary syndrome (PCOS) is associated with insulin resistance and abnormal glucose tolerance. Iron overload may lead also to insulin resistance and diabetes. Serum ferritin levels are increased in PCOS, especially when glucose tolerance is abnormal, suggesting mild iron overload. Factors contributing to potential iron overload in PCOS include the iron sparing effect of chronic menstrual dysfunction, insulin resistance, and a decrease in hepcidin leading to increased iron absorption. Enhancement of erythropoiesis by androgen excess is unlikely, because soluble transferrin receptor levels are not increased in PCOS. Future venues of research should address the long-term effects of PCOS treatment on iron overload and, conversely, the possible effects of iron lowering strategies on the glucose tolerance of patients with PCOS. cellular storage protein for iron, is also an acute phase protein and, hence, serves as a clinical marker of body iron content after significant inflammation has been excluded. forms soluble complexes with hemoglobin after processes of intravascular hemolysis, ameliorating the generation of oxygen reactive species and oxidative stress that might follow the liberation of free iron into the circulation. also called iron overload, is a disorder that results in too much iron being absorbed from the gastrointestinal tract. Patients with hemochromatosis have hyperferritinemia. hormone that acts as the main negative regulator of iron metabolism by inducing the internalization and degradation of the iron transporter ferroportin, thereby reducing intestinal absorption of iron and inhibiting the release of iron from macrophages. protein that forms complexes with transferrin receptor and reduces the release of iron from TfR–diferric transferrin complexes within the endosome. Mutations in HFE gene are responsible for most cases of hereditary hemochromatosis. indicates high serum ferritin levels found in genetic and acquired conditions, that may or may not be associated with iron overload. Patients with hyperferritinemia do not necessarily have hemochromatosis. trace element essential for human life, participates in many reactions because of its ability to cycle from ferrous to ferric forms. Free iron is highly toxic because of the potential for generating free radicals by Fenton reaction. iron transporter in the circulation, may bind one or two ferric ions. binds diferric transferrin in a complex that enters the cell by endocytosis. A soluble form (sTfR) is released into the circulation when the receptor is not bound to diferric transferrin, and serves as a marker of the rate of erythropoiesis. ratio of plasma iron to transferrin (usually between 20% and 50%), increases as a function of iron burden.