Abstract
The role of iron transport proteins in the pathogenesis of anemia in patients with diabetes mellitus (T2DM) is still unclear. We investigated the expression of duodenal transporter proteins in diabetic patients with and without iron deficiency anemia (IDA). Methods. Overall, 39 patients were included: 16 with T2DM and IDA (group A), 11 with T2DM without IDA (group B), and 12 controls (group C). Duodenal mucosal expression of divalent metal transporter 1 (DMT1), ferroportin 1 (FPN), hephaestin (HEPH), and transferrin receptor 1 (TfR) was evaluated by Western blotting. Chronic disease activity markers were measured as well. Results. FPN expression was increased in group A compared to group B and controls: 1.17 (0.72–1.46), 0.76 (0.53–1.04), and 0.71 (0.64–0.86), respectively (p = 0.011). TfR levels were over expressed in groups A and B compared to controls: 0.39 (0.26–0.61), 0.36 (0.24–0.43), and 0.18 (0.16–0.24), respectively, (p = 0.004). The three groups did not differ significantly with regard to cellular HEPH and DMT1 expression. The normal CRP and serum ferritin levels, accompanied with normal FPN among diabetic patients without IDA, do not support the association of IDA with chronic inflammatory state. Conclusion. In patients with T2DM and IDA, duodenal iron transport protein expression might be dependent on body iron stores rather than by chronic inflammation or diabetes per se.
Highlights
Iron absorption by the proximal small bowel is a critical checkpoint in the maintenance of whole-body iron level, as no regulated excretory systems exist for iron in humans [1]
Ferritin has been proposed to be a component of insulin resistance syndrome, as higher heme iron intake and ferritin are associated with a greater risk of type 2 diabetes mellitus (T2DM) [2]
No significant differences were found in HbA1C% between patients with T2DM with or without iron deficiency anemia (IDA)
Summary
Iron absorption by the proximal small bowel is a critical checkpoint in the maintenance of whole-body iron level, as no regulated excretory systems exist for iron in humans [1]. The estimated prevalence of anemia in diabetic patients is about 10% to 30% [3], while approximately one-third exhibit iron deficiency. Any inflammatory conditions are often associated with significant changes in systemic iron metabolism, with altered metabolic state as there is a decrease in plasma iron levels due to reduced intestinal absorption and increased intracellular sequestration of the metal [5]. T2DM, one of the most prevalent chronic inflammatory diseases worldwide, is associated with cytokine secretion that simultaneously increases transferrin receptors (TfR) on the cell surface. The inflammatory cytokines induce hepcidine (HEPC) overproduction which causes the endocytosis and proteolysis of ferroportin (FPN), favoring trapping iron in the absorbing enterocytes resulting in iron deficiency anemia (IDA) [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
