Duodenal Ferroportin Is Up-Regulated in Patients with Chronic Hepatitis C |
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| Authors: | Lanqing Ma Tong Zou Yuping Yuan Jiajun Lv Xiangqian Dong Gang Yang Yunzhen Zhu Juan Luo Zhigang Zhang Jiefu Yang |
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| Institution: | 1. Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University, Kunming, Yunnan, China.; 2. Department of Cardiology, Beijing Hospital, Ministry of Health, Beijing, China.; 3. State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, CAS, Kunming, Yunnan, China.; University of Malaya, Malaysia, |
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| Abstract: | Hepatitis C virus (HCV) infection is a leading cause of liver-related mortality. Chronic hepatitis C (CHC) is frequently associated with disturbances in iron homeostasis, with serum iron and hepatic iron stores being elevated. Accumulating evidence indicates that chronic HCV infection suppresses expression of hepatic hepcidin, a key mediator of iron homeostasis, leading to iron overload conditions. Since hepcidin mediates degradation of ferroportin, a basolateral transporter involved in the release of iron from cells, diminished hepcidin expression probably leads to up-regulation of ferroportin-1 (Fpn1) in patients with CHC. In this study, we determined the protein levels of duodenal Fpn1, and found that its expression was significantly up-regulated in patients with CHC. The expression of duodenal Fpn1 is negatively correlated with mRNA levels of hepcidin, and positively correlated with serum iron parameters. Although iron is a critical factor for growth of a variety of pathogenic bacteria, our results suggest that iron overload in blood does not increase the infection rate of bacteria in patients with CHC. |
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