Impact of Long Term Metformin Therapy on Hepcidin and Iron Status in Type II Diabetic Patients

Abstract

Background /Aims: Diabetes and its complications are considered as a major public health problem in the world and the prevention of these complications has become a public health priority. The recent discovery of hepcidin, the central regulatory molecule of systemic iron homeostasis, changed the view of iron metabolism, which is long known to be linked with insulin resistant status in type 2 diabetes mellitus. Thus, the aim of the current study was to elucidate the impact of metformin administration for long time on iron regulator hepcidin and iron metabolic parameters (Hb, ferritin, TIBC) in Type 2 diabetic patients. Subjects Methods: This study included 45 subjects of both sexes, the age between 35-60 years. Thirty cases with type 2 diabetes who divided into two groups: L-group, treated with metformin for less than 5 years and A-group, treated with metformin for more than 5 years. These groups were compared with the healthy sex and age matched control group (n=15). Fasting blood glucose (FBG), serum insulin, blood hemoglobin (Hb), serum hepcidin, ferritin, Iron and total iron binding capacity (TIBC) have been carried out. Results: The present results recorded highly significant increase in serum hepcidin level in A-group and significant increase in L-group versus the control group. Serum insulin group as well as serum insulin, ferritin and TIBC levels showed highly significant increase in A-group with insignificant increase in L-grouprelative to the control group. Significant depletion in blood Hb as well as in serum iron levels were demonstrated in both A-and L-group with respect to the controlgroup. Hepcidin showed a significant positive correlation with FBG, insulin and ferritin in both diabetic groups (A-and L-group), while it showed a negative correlation with HB and serum iron. Conclusion: The current study provided an evidence for that metformin administration in Type 2 diabetic patients for long time (more than 5 years) caused anima, heperferritinemia, iron deficiency as well as marked increase in serum hepcidin indicating iron overload in liver of these patients.