Alcohol withdrawal is associated with a rebound increase in hepcidin expression: further evidence for an alcohol/hepcidin interaction

Tan, T. C. H., Heritage, M., Jaskowski, L. A., Murphy, T. L., Crawford, D. H. G. and Fletcher, L. M. (2009). Alcohol withdrawal is associated with a rebound increase in hepcidin expression: further evidence for an alcohol/hepcidin interaction. In: Abstracts of the Australia & New Zealand Medical & Surgical Gastrointestinal Week 2009. Australia & New Zealand Medical & Surgical Gastrointestinal Week 2009, Sydney, NSW, Australia, (A275-A275). 21-24 October 2009. doi:10.1111/j.1440-1746.2009.06055.x


Author Tan, T. C. H.
Heritage, M.
Jaskowski, L. A.
Murphy, T. L.
Crawford, D. H. G.
Fletcher, L. M.
Title of paper Alcohol withdrawal is associated with a rebound increase in hepcidin expression: further evidence for an alcohol/hepcidin interaction
Conference name Australia & New Zealand Medical & Surgical Gastrointestinal Week 2009
Conference location Sydney, NSW, Australia
Conference dates 21-24 October 2009
Proceedings title Abstracts of the Australia & New Zealand Medical & Surgical Gastrointestinal Week 2009   Check publisher's open access policy
Journal name Journal of Gastroenterology and Hepatology   Check publisher's open access policy
Place of Publication Richmond, VIC, Australia
Publisher Wiley-Blackwell Publishing Asia
Publication Year 2009
Sub-type Published abstract
DOI 10.1111/j.1440-1746.2009.06055.x
ISSN 0815-9319
1440-1746
Volume 24
Issue Supp. 2
Start page A275
End page A275
Total pages 1
Language eng
Formatted Abstract/Summary
Background: Recent evidence suggests that alcohol causes downregulation of hepcidin expression possibly via inflammatory cytokines, hypoxia and reactive oxygen species, but the time course of this effect is unknown. The effect of alcohol withdrawal on hepcidin gene expression and its transcription factors is unknown, but a rebound response would provide further evidence that alcohol alters hepcidin gene expression.

Aim: To further examine the hypothesis that alcohol causes downregulation of hepcidin by studying the time course of the alcohol effects and the response to alcohol withdrawal.

Methods: C57BL/6 mice were pair fed alcohol-Lieber de Carli diets or control equivalents without alcohol. 12 mice were in the ethanol treatment arm and 12 were in the control diet arm. Alcohol-Lieber deCarli was given over a period of 6 weeks in the study arm. At the end of the 6 weeks the alcohol treated mice had their diets reverted to the control Lieber deCarli without alcohol for a further 4 weeks. Levels of gene and protein expression of hepcidin (hamp1), and the transcription factors C/EBPa and
STAT3 were measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis and Western blotting respectively at week 4, 6 and 10. Expression of intestinal iron absorption genes DMT1 and ferroportin were also measured by RT-PCR.

Results: Compared to mice on control diet, hepcidin RNA expression was reduced in alcohol treated mice although this effect was not evident until after 6 weeks of treatment. Contrary to other reports, there was an increase in pSTAT3 and CEBPa in the wild type mice following ethanol consumption. Consistent with previous reports the expression of ferroportin was upregulated by alcohol but this was not statistically significant (P = 0.38) and not evident until after at least 4 weeks of treatment. Levels of
DMT1 expression did not alter significantly with alcohol treatment or withdrawal (P = 0.45 and P = 0.68). When the alcohol was ceased, there was a significant rebound upregulation with almost doubling of hepcidin expression (P = 0.002). This observation was not accompanied by a rise in CEBPa or STAT3 expression, nor any change in the expression of intestinal iron transporters.

Conclusion: This study further confirms previous findings that alcohol causes down regulation of hepcidin expression with the effect apparent after 6 weeks of treatment. The rebound in hepcidin expression following alcohol withdrawal provides further evidence of an alcohol—hepcidin interaction.
Q-Index Code CX
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes Article first published online: 5 OCT 2009

Document type: Conference Paper
Collection: School of Medicine Publications
 
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Created: Sun, 13 Dec 2009, 00:03:54 EST