ArticleHepatology (Baltimore, Md.)2012
Lower serum hepcidin and greater parenchymal iron in nonalcoholic fatty liver disease patients with C282Y HFE mutations.
Article in Hepatology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Association between pattern of hepatic iron deposition and severity of MASH among patients enrolled in the NASH Clinical Research Network.Hepatology communications · 2025Article
- Interplay between gut microbiota and the master iron regulator, hepcidin, in the pathogenesis of liver fibrosis.Pathogens and disease · 2024Review
- Genetic variants in HFE are associated with non-alcoholic fatty liver disease in lean individuals.JHEP reports : innovation in hepatology · 2023Article
- The role of regulated necrosis in endocrine diseases.Nature reviews. Endocrinology · 2021Review
- Ironing Out the Details: How Iron Orchestrates Macrophage Polarization.Frontiers in immunology · 2021Review
- Hepcidin levels correlate to liver iron content, but not steatohepatitis, in non-alcoholic fatty liver disease.BMC gastroenterology · 2018Article
- Dietary Iron Supplementation Alters Hepatic Inflammation in a Rat Model of Nonalcoholic Steatohepatitis.Nutrients · 2018Article
- Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease.Oxidative medicine and cellular longevity · 2018Review
- Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease.Biomedical reports · 2017Article
- Iron and non-alcoholic fatty liver disease.World journal of gastroenterology · 2016Review
- The Role of Iron and Iron Overload in Chronic Liver Disease.Medical science monitor : international medical journal of experimental and clinical research · 2016Review
- Serum adipokines might predict liver histology findings in non-alcoholic fatty liver disease.World journal of gastroenterology · 2016Observational
- Heterozygous Hfe gene deletion leads to impaired glucose homeostasis, but not liver injury in mice fed a high-calorie diet.Physiological reports · 2016Article
- Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver.World journal of hepatology · 2016Article
- Prediction of Nonalcoholic Fatty Liver Disease Via a Novel Panel of Serum Adipokines.Medicine · 2016Article
- Article
- Saturated fatty acids induce post-transcriptional regulation of HAMP mRNA via AU-rich element-binding protein, human antigen R (HuR).The Journal of biological chemistry · 2015Article
- Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver.World journal of hepatology · 2015Review
- Systematic review of genetic association studies involving histologically confirmed non-alcoholic fatty liver disease.BMJ open gastroenterology · 2015Article
- Role of liver biopsy in nonalcoholic fatty liver disease.World journal of gastroenterology · 2014Review
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4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledHepcidin regulation is linked to both iron and inflammatory signals and may influence iron loading in nonalcoholic steatohepatitis (NASH). The aim of this study was to examine the relationships among HFE genotype, serum hepcidin level, hepatic iron deposition, and histology in nonalcoholic fatty liver disease (NAFLD). Single-nucleotide polymorphism genotyping for C282Y (rs1800562) and H63D (rs1799945) HFE mutations was performed in 786 adult subjects in the NASH Clinical Research Network (CRN). Clinical, histologic, and laboratory data were compared using nonparametric statistics and multivariate logistic regression. NAFLD patients with C282Y, but not H63D mutations, had lower median serum hepcidin levels (57 versus 65 ng/mL; P = 0.01) and higher mean hepatocellular (HC) iron grades (0.59 versus 0.28; P < 0.001), compared to wild-type (WT) subjects. Subjects with hepatic iron deposition had higher serum hepcidin levels than subjects without iron for all HFE genotypes (P < 0.0001). Hepcidin levels were highest among patients with mixed HC/reticuloendothelial system cell (RES) iron deposition. H63D mutations were associated with higher steatosis grades and NAFLD activity scores (odds ratio [OR], ≥1.4; 95% confidence interval [CI]: >1.0, ≤2.5; P ≤ 0.041), compared to WT, but not with either HC or RES iron. NAFLD patients with C282Y mutations had less ballooning or NASH (OR, ≤0.62; 95% CI: >0.39, <0.94; P ≤ 0.024), compared to WT subjects.
conclusionsThe presence of C282Y mutations in patients with NAFLD is associated with greater HC iron deposition and decreased serum hepcidin levels, and there is a positive relationship between hepatic iron stores and serum hepcidin level across all HFE genotypes. These data suggest that body iron stores are the major determinant of hepcidin regulation in NAFLD, regardless of HFE genotype. A potential role for H63D mutations in NAFLD pathogenesis is possible through iron-independent mechanisms.
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