{'fraction_non_alphanumeric': 0.03524904214559387, 'fraction_numerical': 0.024521072796934867, 'mean_word_length': 5.433497536945813, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Differential expression of iron metabolism proteins in diabetic and diabetic iron‐supplemented rat liver

Diabetes mellitus is associated with altered iron homeostasis that can potentially effect reactive oxygen species generation and contribute to diabetes‐related complications. We investigated, by quantitative polymerase chain reaction, whether the expression of liver hepcidin, ferritin, and TfR‐1 is altered in diabetes. Rats in the control (C) group received a standard diet; control iron (CI) group received a standard diet supplemented with iron; diabetic (D) group received an injection of streptozotocin; and diabetic iron (DI) group received streptozotocin and the diet with iron. Animals of the D group showed higher levels of serum iron, increased concentration of carbonyl protein, and a decrease in antioxidant status. Group D rats showed increased hepatic expression of Trf‐1 compared to the other groups. Iron supplementation reversed this increase. Hepcidin mRNA was 81% higher in DI than in C and CI rats. The results suggest that diabetes, with or without excess iron, can cause perturbations in iron status, hepcidin and Trf‐1 expression. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:123–129, 2012; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20418