Background and aim: Studies suggest that iron plays a significant role in the development of diabetes and its complications. This study evaluates the associations of iron metabolism parameters with the metabolic syndrome (MS), control and complications in female patients with type 2 diabetes mellitus (T2DM).
Methods and results: Ferritin, soluble Transferrin Receptor (sTfR), sTfR/Log ferritin ratio (sTfR-F index), iron, full blood count and high-sensitivity C-reactive protein (hs-CRP) were determined in 110 female patients with T2DM. Steady state beta cell function (%B), insulin sensitivity (%S) and insulin resistance were assessed with homeostasis model. Patients were divided into tertiles of ferritin and sTfR-F index and according to the presence or absence of the MS and diabetic complications. Patients within the lowest tertile of the sTfR-F index had significantly higher fasting insulin, percent B, low-density lipoprotein cholesterol and Apolipoprotein B than those in the highest tertile. Ferritin showed significant correlations with insulin, percent B and inverse correlations with adiponectin and percent S. The sTfR-F index was significantly correlated with insulin, percent B and lipid parameters. Correcting for hs-CRP abolished the correlations with ferritin but not the sTfR-F index. Higher indices of body iron were significantly associated with diabetes complications but no associations were found with MS, glucose or glycemic control. Multiple regression analysis with confounding variables showed ferritin and the sTfR-F index were not independently associated with diabetes complications.
Conclusions: Association of ferritin with metabolic derangements and complications in diabetes is partly dependent on association with inflammation. Iron status, estimated with the sTfR-F index, is associated with metabolic derangements and complications but the associations are dependent on other risk factors. Prospective studies that use the sTfR-F index as a marker of iron status are required to confirm the role of iron in the etiopathogenesis of T2DM and its complications.