Abstract
Backgrounds and aimBesides the clinical evidence supporting insulin resistance in chronic hepatitis C (CHC) patients, the exact mechanism elucidating insulin resistance is still under discussion. The present study aimed to observe any relationship between serum hepcidin, serum iron, and insulin resistance in CHC patients.MethodologyA total of 54 individuals were recruited in this study, assorted into group A (CHC population with diabetes) and control group B (CHC population without diabetes). Both groups were tested for serum hepcidin, iron, ferritin, and serum glycemic indices (fasting blood glucose, serum insulin, and insulin resistance). Serum parameters were compared between diabetic and non-diabetic CHC patients by using the Mann-Whitney U test. Correlation analysis was done between serum hepcidin and serum iron, serum hepcidin, and insulin resistance, and serum iron and insulin resistance by applying the Spearman correlation test.ResultsDiabetic and non-diabetic CHC populations exhibited an iron profile of chronic illness, i.e., low serum iron and hepcidin along with normal ferritin levels. Also, the diabetic and non-diabetic CHC population exhibited normal serum insulin and insulin resistance. However, the fasting serum glucose of the diabetic CHC population was higher than normal. Correlation analysis indicated a negative significant correlation (rho=-0.404, p=0.036) between serum iron and insulin resistance among the diabetic CHC population.ConclusionOur study could not provide any mounting evidence in favor of insulin resistance in the chronic hepatitis C population via serum iron or hepcidin. Hepatitis C virus causing diabetes mellitus may have some etiology other than iron metabolism.
Highlights
The liver has a special role to play in iron homeostasis by influencing iron uptake, storage, transport, and mobilization from storage to maintain erythropoietic demands [1]
Chronic hepatitis C virus (HCV) infection is a prevalent cause of iron overload by enhanced expression of core+1/alternate reading frame protein (ARFP) induced inhibition of hepcidin promoter and hepcidin transcription [5]
The present study was conducted to assess the link between chronic hepatitis C (CHC) and insulin resistance via serum hepcidin and serum iron levels
Summary
The liver has a special role to play in iron homeostasis by influencing iron uptake, storage, transport, and mobilization from storage to maintain erythropoietic demands [1]. Adequate iron stores in blood signal for increased hepatic expression of hepcidin and internalization of ferroportin, preventing the iron efflux from enterocytes and vice versa. Chronic hepatitis C virus (HCV) infection is a prevalent cause of iron overload by enhanced expression of core+1/alternate reading frame protein (ARFP) induced inhibition of hepcidin promoter and hepcidin transcription [5]. Another HCV protein, nonstructural protein 5A (NS5A) decreases the hepcidin expression by inhibiting its messenger RNA, increasing iron stores and its deposition in hepatocytes and macrophages [6, 7]
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