Diabetes mellitus, a chronic, metabolic disorder characterized by insulin resistance and impaired glucose homeostasis [1], has contributed tremendously to the burden of mortality and disability worldwide [2]. The epidemic of diabetes mellitus and its complications pose a major global health threat. Recently, Type 2 Diabetes (T2DM) has been linked to ferroptosis, a form of nonapoptotic regulated cell death that was first defined in 2012. Notably, ferroptosis is dependent on intracellular iron and insulin secretion dysfunction in pancreatic β-cells [3]. Iron is an indispensable element for metabolic reactions as it is involved in protein synthesis and imbalance in iron metabolism both overload or deficiency can affect vital physiological pathways [4]. Therefore, balanced iron metabolism in the body is an obligatory need of the body to perform metabolic functions properly. Taken together, the monitoring and control of iron metabolism and ferroptosis-related factors may facilitate early diagnosis and therapy of T2DM. However, to date, only a small number of studies have explored the relationship between iron metabolism, ferroptosis, and T2DM.

Developing disease-modifying therapeutics for T2DM necessitates the identification of appropriate pharmacological targets and therapeutic effectiveness measures. To further understand the function of ferroptosis in T2DM in pancreatic -cells and immune effector cells, information on dysregulation, if any, in expression of genes linked with iron metabolism in the context of T2DM, in relevant effector cells is required. Human invasive tissue samples are difficult to collect [5]. However, islet-infiltrating immune effectors are probably in balance with circulating pools and may be collected in peripheral blood mononuclear cells (PBMCs) [6,7].

In this study, we hypothesize that information on the status of iron metabolism associated metabolism might be reflected in the expression of iron metabolism genes in PBMCs. As such, the aim of this study was to assess the expression of genes linked with iron metabolism (Ferritin Light Chain, FTL; Ferritin Heavy Chain, FTH1; Transferrin Receptor, TFRC; Divalent Metal Transporter 1, SLC11A2; Ferroportin, SLC40A1) in PBMCs from T2DM patients and investigate relations between expression of iron metabolism genes in PBMCs with the anthropometric and clinical parameters of the T2DM patients.

Iron is one of the important trace mineral elements involved in several metabolic processes needed to life [8]. A recent study had indicated the role of iron in islet functions under diabetic conditions in human islet amyloid polypeptide-induced diabetes mouse model, and reports that decreased iron level was associated with the dysregulation of glucose stimulated mitochondrial respiration [9]. Also, the body’s ferritin level is closely related to ferroptosis. The probable link between increased body iron accumulation and T2DM has been identified by epidemiological investigations [3]. In this view, monitoring changes in the gene expression of iron metabolism markers in PBMCs from T2DM patients may be a crucial first step in understanding how iron metabolism is affected in T2DM patients.