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Obesity Promotes Alterations in Iron Recycling

Hepcidin is a key hormone that induces the degradation of ferroportin (FPN), a protein that exports iron from reticuloendothelial macrophages and enterocytes. The aim of the present study was to experimentally evaluate if the obesity induced by a high-fat diet (HFD) modifies the expression of FPN in...

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Autores principales: Citelli, Marta, Fonte-Faria, Thaís, Nascimento-Silva, Vany, Renovato-Martins, Mariana, Silva, Raphael, Luna, Aderval Severino, Vargas da Silva, Simone, Barja-Fidalgo, Christina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303843/
https://www.ncbi.nlm.nih.gov/pubmed/25569627
http://dx.doi.org/10.3390/nu7010335
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author Citelli, Marta
Fonte-Faria, Thaís
Nascimento-Silva, Vany
Renovato-Martins, Mariana
Silva, Raphael
Luna, Aderval Severino
Vargas da Silva, Simone
Barja-Fidalgo, Christina
author_facet Citelli, Marta
Fonte-Faria, Thaís
Nascimento-Silva, Vany
Renovato-Martins, Mariana
Silva, Raphael
Luna, Aderval Severino
Vargas da Silva, Simone
Barja-Fidalgo, Christina
author_sort Citelli, Marta
collection PubMed
description Hepcidin is a key hormone that induces the degradation of ferroportin (FPN), a protein that exports iron from reticuloendothelial macrophages and enterocytes. The aim of the present study was to experimentally evaluate if the obesity induced by a high-fat diet (HFD) modifies the expression of FPN in macrophages and enterocytes, thus altering the iron bioavailability. In order to directly examine changes associated with iron metabolism in vivo, C57BL/6J mice were fed either a control or a HFD. Serum leptin levels were evaluated. The hepcidin, divalent metal transporter-1 (DMT1), FPN and ferritin genes were analyzed by real-time polymerase chain reaction. The amount of iron present in both the liver and spleen was determined by flame atomic absorption spectrometry. Ferroportin localization within reticuloendothelial macrophages was observed by immunofluorescence microscopy. Obese animals were found to exhibit increased hepcidin gene expression, while iron accumulated in the spleen and liver. They also exhibited changes in the sublocation of splenic cellular FPN and a reduction in the FPN expression in the liver and the spleen, while no changes were observed in enterocytes. Possible explanations for the increased hepcidin expression observed in HFD animals may include: increased leptin levels, the liver iron accumulation or endoplasmic reticulum (ER) stress. Together, the results indicated that obesity promotes changes in iron bioavailability, since it altered the iron recycling function.
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spelling pubmed-43038432015-02-02 Obesity Promotes Alterations in Iron Recycling Citelli, Marta Fonte-Faria, Thaís Nascimento-Silva, Vany Renovato-Martins, Mariana Silva, Raphael Luna, Aderval Severino Vargas da Silva, Simone Barja-Fidalgo, Christina Nutrients Article Hepcidin is a key hormone that induces the degradation of ferroportin (FPN), a protein that exports iron from reticuloendothelial macrophages and enterocytes. The aim of the present study was to experimentally evaluate if the obesity induced by a high-fat diet (HFD) modifies the expression of FPN in macrophages and enterocytes, thus altering the iron bioavailability. In order to directly examine changes associated with iron metabolism in vivo, C57BL/6J mice were fed either a control or a HFD. Serum leptin levels were evaluated. The hepcidin, divalent metal transporter-1 (DMT1), FPN and ferritin genes were analyzed by real-time polymerase chain reaction. The amount of iron present in both the liver and spleen was determined by flame atomic absorption spectrometry. Ferroportin localization within reticuloendothelial macrophages was observed by immunofluorescence microscopy. Obese animals were found to exhibit increased hepcidin gene expression, while iron accumulated in the spleen and liver. They also exhibited changes in the sublocation of splenic cellular FPN and a reduction in the FPN expression in the liver and the spleen, while no changes were observed in enterocytes. Possible explanations for the increased hepcidin expression observed in HFD animals may include: increased leptin levels, the liver iron accumulation or endoplasmic reticulum (ER) stress. Together, the results indicated that obesity promotes changes in iron bioavailability, since it altered the iron recycling function. MDPI 2015-01-06 /pmc/articles/PMC4303843/ /pubmed/25569627 http://dx.doi.org/10.3390/nu7010335 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Citelli, Marta
Fonte-Faria, Thaís
Nascimento-Silva, Vany
Renovato-Martins, Mariana
Silva, Raphael
Luna, Aderval Severino
Vargas da Silva, Simone
Barja-Fidalgo, Christina
Obesity Promotes Alterations in Iron Recycling
title Obesity Promotes Alterations in Iron Recycling
title_full Obesity Promotes Alterations in Iron Recycling
title_fullStr Obesity Promotes Alterations in Iron Recycling
title_full_unstemmed Obesity Promotes Alterations in Iron Recycling
title_short Obesity Promotes Alterations in Iron Recycling
title_sort obesity promotes alterations in iron recycling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303843/
https://www.ncbi.nlm.nih.gov/pubmed/25569627
http://dx.doi.org/10.3390/nu7010335
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