Marmur J, et al. - Researchers investigated whether body iron stores, steatohepatitis or lipid status in non-alcoholic fatty liver disease (NAFLD) associated with hepcidin synthesis. Findings revealed that serum hepcidin and hepcidin antimicrobial peptide (HAMP) mRNA in liver correlated to body iron content but not to the degree of steatohepatitis or lipid status in NAFLD with or without dysmetabolic iron overload. Data reported that the dysmetabolic iron overload syndrome (DIOS) observed in NAFLD was not caused by an altered hepcidin synthesis.

Methods

• For this analysis, 84 patients with liver disease, 54 of which had iron overload, underwent liver biopsy (n = 66) and/or magnetic resonance imaging (n = 35) for liver iron content determination.
• Thirty-eight of the patients had NAFLD, 29 had chronic liver disease other than NAFLD, and 17 had untreated genetic hemochromatosis.
• In all patients and in 34 controls, serum hepcidin was measured with ELISA.
• With real-time-quantitative PCR, hepcidin antimicrobial peptide (HAMP) mRNA in liver tissue was determined in 36 patients.

Results

• The study results showed that serum hepcidin was increased similarly in NAFLD with DIOS as in the other chronic liver diseases with iron overload, except for genetic hemochromatosis.
• Findings revealed that HAMP mRNA in liver tissue, and serum hepcidin, both correlated to liver iron content in NAFLD patients (r² = 0.45, p < 0.05 and r² = 0.27, p < 0.05 respectively) but not to body mass index, NAFLD activity score or serum lipids.
• A good correlation between HAMP mRNA in liver tissue and serum hepcidin (r² = 0.39, p < 0.01) was found.