Abstract
Objective. We aimed to analyze the alterations of activity of iron metabolism members i.e. ceruloplasmin (Cp) and transferrin (Tf), in relation to the percentage of glycated hemoglobin. The latter is one of biochemical criteria of chronic hyperglycemia compensation in case of type 2 diabetes mellitus.
 Materials and methods. Concentration and activity of Cp and Tf, concentration of iron, copper and lipoprotein cholesterol were measured by biochemical methods in blood serum samples obtained from healthy donors and patients with type 2 diabetes mellitus divided in three groups according to glycated hemoglobin level.
 Results. The significant decrease in serum copper, ferroxidase activity of Cp and iron-binding capacity of Tf, as well as an increase of Tf concentration, in groups with compensated and uncompensated type 2 diabetes mellitus was found.
 Conclusion. Our data demonstrate a statistical link between the degree of type 2 diabetes mellitus compensation and alteration of iron metabolism members’ activity. Thus, an increase of hyperglycemia is associated with a decrease of both Cp ferroxidase activity and the degree of Tf saturation with iron. These alterations may explain the efficiency of treatment with iron chelators of such type 2 diabetes mellitus complications as trophic ulcers. The said disease condition is directly connected with the changes in iron efflux.
Highlights
Type 2 diabetes mellitus (T2D) is associated with iron metabolism disorders, including those of hereditary etiology [1]
T2D is found in about 80% of cases of hereditary hemochromatosis, which is associated with mutations in genes controlling iron metabolism: HFE, HAMP, TFR2, SLC40A1, and HFE2 [1]
Taking into account that alteration of Cp ferroxidase activity in case of hereditary pathology of copper metabolism is usually compensated by low-density lipoprotein (LDL)‐associated ferroxidase activity [13], the study of the link between T2D and cholesterol level can be informative
Summary
Type 2 diabetes mellitus (T2D) is associated with iron metabolism disorders, including those of hereditary etiology [1]. T2D is found in about 80% of cases of hereditary hemochromatosis, which is associated with mutations in genes controlling iron metabolism: HFE (hemochromatosis protein), HAMP (hepcidin), TFR2 (transferrin receptor), SLC40A1 (ferroportin), and HFE2 (hemojuvelin) [1]. Diminution of Cp activities due to aggregation, losing of copper ions and the decreasing ferroxidase activity after in vitro modification by methylglyoxal or aminoacetone has been shown. The latter metabolites’ levels are elevated in blood plasma in T2D patients [5, 6]. The level of the so-called non-ceruloplasmin copper is increased in blood serum of T2D patients [7]. Taking into account that alteration of Cp ferroxidase activity in case of hereditary pathology of copper metabolism is usually compensated by low-density lipoprotein (LDL)‐associated ferroxidase activity [13], the study of the link between T2D and cholesterol level can be informative
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