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Long‐Term Dexamethasone Exposure Down‐Regulates Hepatic TFR1 and Reduces Liver Iron Concentration in Rats
Author(s) -
Huifang Li
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.826.1
Subject(s) - medicine , endocrinology , transferrin receptor , dmt1 , dexamethasone , chemistry , transferrin , hepcidin , ferroportin , corticosterone , oxidative stress , transporter , anemia , hormone , biochemistry , gene
Exposure to stress is known to cause hepatic iron dysregulation, but the relationship between prolonged stress and liver iron metabolism is not yet fully understood. Thirty 13‐week‐old female Sprague–Dawley rats were randomly divided into two groups, as follows: the control group (saline‐injection) and the dexamethasone group (Dexamethasone (Dex)‐injection 0.1 mg/kg/day). After the 21‐day stress trial, the results showed that chronic Dex administration not only impaired serum corticosterone (p = 0.00) and interleukin‐6 (IL‐6) (p = 0.01) levels, but also decreased white blood cell counts (p = 0.00), and reduced blood lymphocyte counts (p = 0.00). The daily Dex‐injection also significantly reduced body weight (p < 0.01) by inhibiting food intake. Consecutive Dex administration resulted in decreased iron intake (p = 0.00), enhanced serum iron levels (p = 0.01), and increased the serum souble transferrin receptor (sTfR) content (p = 0.00) in rats. Meanwhile, long‐term Dex exposure down‐regulated duodenal cytochrome b (DCYTB) (p = 0.00) and the divalent metal transporter 1 (DMT1) (p = 0.04) protein expression, but up‐regulated ferroportin (FPN) protein expression (p = 0.04). Chronic Dex administration reduced liver iron concentration (p = 0.02) in rats. Hepatic transferrin receptor 1 (TFR1) expression was lowered at the protein level (p = 0.03), yet with uncoupled mRNA abundance in Dex‐treated rats. Enhanced iron‐regulatory protein (IRP)/iron‐responsive element (IRE) binding activity was observed, but did not line up with lowered hepatic TFR1 protein expression. This study indicates that long‐term Dex exposure reduces liver iron content, which is closely associated with down‐regulated hepatic TFR1 protein expression. Support or Funding Information This work was supported by grants from the National Natural Science Foundation of China (31302053), the Fundamental Research Funds for the Central Universities (KJQN201404), the Innovation Project of Jiangsu Province Postgraduate Education (2013CXLX13_292), the Priority Academic Program Development of Jiangsu Higher Education Institutions and the Jiangsu Collaborative Innovation Center of Meat Production and Processing, Quality and Safety Control. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .