Iron Deficiency Anemia and Diabetes Mellitus

Iron is necessary for various metabolic processes, including oxygen transport and storage, redox reactions, cell signaling and microbial defense. Absorption, transport and storage of iron are carefully regulated, presumably to avert potential toxic effects of free iron [1,2]. Both iron overload and iron deficiency can be detrimental to health, so iron homeostasis is essential. Although many factors that take part in iron homeostasis are known, mechanisms by which the body regulates iron stores are still being elucidated [1-3]. Also, iron absorption and homeostasis are intimately linked to the inflammatory response [4]. Iron deficiency (ID) and iron deficiency anemia (IDA) are prevalent forms of nutritional deficiency. Globally, 50% of anemia is attributed to iron deficiency [5,6]. Since the body has no means of actively excreting excess iron, a sophisticated system for iron homeostasis maintains the optimal balance between adequate dietary iron absorption and iron loss in healthy individuals. Dietary iron is absorbed in a regulated manner from the gastrointestinal tract and transported between cells bound to the protein transferrin. Systemic iron homeostasis is primarily regulated by the liver-derived peptide hormone hepcidin and by the iron exporter protein ferroprotein, while intracellular iron homeostasis is regulated by the iron-regulatory protein/iron-responsive element system. The two regulatory systems are finely coordinated [7]. This finely balanced homeostasis, however, can be readily disturbed. Iron deficiency can ensue if dietary iron intake is insufficient or if iron absorption, loss, metabolism, or body distribution become abnormal due to disease or excess blood loss. A group of international experts recently proposed the following comprehensive definition of iron deficiency: “a health-related condition in which iron availability is insufficient to meet the body’s needs and which can be present with or without anemia” [8].