Vol. 85, June 2017

The Relation between Serum Hepcidin Level and Cardiometabolic Risk Factors in Experimentally Induced Chronic Renal Failure Rat Model

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The Relation between Serum Hepcidin Level and Cardiometabolic Risk Factors in Experimentally Induced Chronic Renal Failure Rat Model, NAWAL K. GERGES

 


Abstract
Background: Hepcidin, a 25 amino-acid peptide produced mainly in the liver, serves as a key component in the regulation of iron homeostasis. Previous studies stated the possibility that hepcidin may relate to different metabolic disorders in different conditions; however, the association between cardi-ometabolic risk factors (CMRFs) and hepcidin as well as other iron parameters in CRF remains unclear.
Objective: This study was designed to evaluate serum hepcidin levels in relation to kidney function test, inflammatory markers, and iron metabolic parameters in CRF-rat model and to explore their association with cardiometabolic risk factors such as impaired glucose metabolism, dyslipidemia, atherosclerosis, and elevated blood pressure.
Material and Methods: 35 healthy male albino rats weigh-ing 160-210gm were used and divided into two groups: control group (15 rats) and CRF-induced group (20 rats), where CRF was induced by injection of folic acid subcutaneously (300mg /kg once a week) for 5 weeks. Blood samples were taken from the cannula after measuring blood pressure. The separated serum was examined for levels of hepcidin, glucose, insulin, TG, cholesterol, LDL, HDL, urea, creatinine, CRP, IL-6, iron, TIBC and ferritin.
Results: There was a significant increase in serum hepcidin level in CRF-induced group when compared to that of control group. Also there were significant positive correlations between serum hepcidin levels and the significant higher levels of urea, creatinine, proteinuria, glucose, insulin, atherogenic lipid profile (TG, cholesterol, LDL-cholesterol), inflammatory markers (IL6, CRP), serum ferritin, HOMA-IR, atherogenic index, and systolic blood pressure in the CRF-induced group. However, serum levels of HDL-cholesterol, and creatinine clearance were significantly lower and negatively correlated with serum hepcidin levels in the CRF-induced group.
In addition, there was a significant positive correlation between atherogenic index and some parameters; serum levels of glucose, insulin, CRP, IL-6, urea, creatinine, atherogenic lipid profile (TG, cholesterol, LDL-cholesterol), inflammatory markers (IL6, CRP), and calculated HOMA-IR in the CRF-induced group.

Conclusion: Folic acid-induced CRF elevated the serum hepcidin level due to the inflammatory state of renal failure, together with decrease its renal clearance. This higher hepcidin level which was positively correlated with the high level of serum ferritin, aggravated cardiometabolic risk factors such as impaired glucose tolerance, dyslipidemia, atherosclerosis, and elevated blood pressure.

 

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