Hepatic Response of Magnesium-Restricted Wild Type Mice

Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-defic...

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Autores principales: Vera H. Fengler, Tanja Macheiner, Walter Goessler, Maria Ratzer, Johannes Haybaeck, Karine Sargsyan
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/72b6711ff27e495a9d81ad6ea3dc0f7f
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spelling oai:doaj.org-article:72b6711ff27e495a9d81ad6ea3dc0f7f2021-11-25T18:20:44ZHepatic Response of Magnesium-Restricted Wild Type Mice10.3390/metabo111107622218-1989https://doaj.org/article/72b6711ff27e495a9d81ad6ea3dc0f7f2021-11-01T00:00:00Zhttps://www.mdpi.com/2218-1989/11/11/762https://doaj.org/toc/2218-1989Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the hepatic inflammatory response was quantified by determining hepatic IL-6, TNFα, and MCP-1. Magnesium-restriction resulted in at least a 2-fold significant reduction of serum magnesium levels compared to the high-fat-diet fed and control mice, whereas the hepatic magnesium content was decreased due to high-fat-diet feeding. No changes in metabolic markers in magnesium-restricted mice were observed, while the cholesterol content was elevated in high-fat-diet fed mice. Magnesium-restricted mice additionally featured inflammation and enlarged hepatocytes in liver histology. Furthermore, magnesium-restricted and high-fat-diet fed mice exhibited elevated hepatic TNFα levels compared to control mice. Accordingly, our data suggest that magnesium is involved in hepatic inflammatory processes and hepatocyte enlargement, key histological features of human NAFLD, and may therefore contribute to development and progression of the disease.Vera H. FenglerTanja MacheinerWalter GoesslerMaria RatzerJohannes HaybaeckKarine SargsyanMDPI AGarticlemagnesium-restrictionmagnesium-deficiencyexperimental mouse modelnon-alcoholic fatty liver diseasehepatic inflammationhepatic steatosisMicrobiologyQR1-502ENMetabolites, Vol 11, Iss 762, p 762 (2021)
institution DOAJ
collection DOAJ
language EN
topic magnesium-restriction
magnesium-deficiency
experimental mouse model
non-alcoholic fatty liver disease
hepatic inflammation
hepatic steatosis
Microbiology
QR1-502
spellingShingle magnesium-restriction
magnesium-deficiency
experimental mouse model
non-alcoholic fatty liver disease
hepatic inflammation
hepatic steatosis
Microbiology
QR1-502
Vera H. Fengler
Tanja Macheiner
Walter Goessler
Maria Ratzer
Johannes Haybaeck
Karine Sargsyan
Hepatic Response of Magnesium-Restricted Wild Type Mice
description Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the hepatic inflammatory response was quantified by determining hepatic IL-6, TNFα, and MCP-1. Magnesium-restriction resulted in at least a 2-fold significant reduction of serum magnesium levels compared to the high-fat-diet fed and control mice, whereas the hepatic magnesium content was decreased due to high-fat-diet feeding. No changes in metabolic markers in magnesium-restricted mice were observed, while the cholesterol content was elevated in high-fat-diet fed mice. Magnesium-restricted mice additionally featured inflammation and enlarged hepatocytes in liver histology. Furthermore, magnesium-restricted and high-fat-diet fed mice exhibited elevated hepatic TNFα levels compared to control mice. Accordingly, our data suggest that magnesium is involved in hepatic inflammatory processes and hepatocyte enlargement, key histological features of human NAFLD, and may therefore contribute to development and progression of the disease.
format article
author Vera H. Fengler
Tanja Macheiner
Walter Goessler
Maria Ratzer
Johannes Haybaeck
Karine Sargsyan
author_facet Vera H. Fengler
Tanja Macheiner
Walter Goessler
Maria Ratzer
Johannes Haybaeck
Karine Sargsyan
author_sort Vera H. Fengler
title Hepatic Response of Magnesium-Restricted Wild Type Mice
title_short Hepatic Response of Magnesium-Restricted Wild Type Mice
title_full Hepatic Response of Magnesium-Restricted Wild Type Mice
title_fullStr Hepatic Response of Magnesium-Restricted Wild Type Mice
title_full_unstemmed Hepatic Response of Magnesium-Restricted Wild Type Mice
title_sort hepatic response of magnesium-restricted wild type mice
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/72b6711ff27e495a9d81ad6ea3dc0f7f
work_keys_str_mv AT verahfengler hepaticresponseofmagnesiumrestrictedwildtypemice
AT tanjamacheiner hepaticresponseofmagnesiumrestrictedwildtypemice
AT waltergoessler hepaticresponseofmagnesiumrestrictedwildtypemice
AT mariaratzer hepaticresponseofmagnesiumrestrictedwildtypemice
AT johanneshaybaeck hepaticresponseofmagnesiumrestrictedwildtypemice
AT karinesargsyan hepaticresponseofmagnesiumrestrictedwildtypemice
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