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Novel pathway for iron deficiency in pediatric non‐alcoholic steatohepatitis (1042.1)
Author(s) -
Moya Diana,
Baker Susan,
Liu Wensheng,
Garrick Michael,
Kozielski Rafal,
Baker Robert,
Zhu Lixin
Publication year - 2014
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.28.1_supplement.1042.1
Subject(s) - transferrin , transferrin receptor , ferritin , steatohepatitis , iron deficiency , medicine , endocrinology , carbohydrate deficient transferrin , soluble transferrin receptor , chemistry , fatty liver , biochemistry , anemia , disease , iron status , alcohol , alcohol consumption
Non‐alcoholic steatohepatitis (NASH) is an obesity related liver disease characterized by steatosis and inflammation. Iron may play a role in NASH pathology as it catalyzes the production of reactive oxygen species. To examine the iron status in pediatric NASH, serum iron, ferritin, and soluble transferrin receptor 1 in NASH patients were compared to those in the National Health and Nutrition Examination Survey database. Serum iron and soluble transferrin receptor 1 were decreased while serum ferritin was increased in NASH patients. No detectable iron was observed in NASH liver by Perls’ Prussian blue staining. Microarray and quantitative real‐time PCR indicated that the mRNA of transferrin, transferrin receptor 2 and catalase were significantly elevated in NASH patients, and that transferrin mRNA was positively correlated with catalase mRNA. To test the hypothesis that oxidative stress induces iron deficiency, HepG2 cells were treated with H 2 O 2 , and the mRNA of transferrin and catalase were induced and positively correlated. We conclude that there is a tendency towards iron deficiency in pediatric NASH patients. Increased liver gene expression of transferrin and transferrin receptor 2 supports a status of iron deficiency. Our finding that H 2 O 2 induces the expression of transferrin, and consequently, decreased iron absorption, suggests a novel mechanism for iron deficiency in NASH patients.