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Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet

Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In the present study, the contribution of TNX to liver dysfunction was investigated by administration of high-fat and high-cholesterol diet with high levels of phosphorus and calcium (HFCD) to wild-type...

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Autores principales: Yamaguchi, Shinsaku, Kawakami, Kohei, Satoh, Kazumi, Fukunaga, Naoki, Akama, Kazuhito, Matsumoto, Ken-Ichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5646988/
https://www.ncbi.nlm.nih.gov/pubmed/28731143
http://dx.doi.org/10.3892/mmr.2017.7052
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author Yamaguchi, Shinsaku
Kawakami, Kohei
Satoh, Kazumi
Fukunaga, Naoki
Akama, Kazuhito
Matsumoto, Ken-Ichi
author_facet Yamaguchi, Shinsaku
Kawakami, Kohei
Satoh, Kazumi
Fukunaga, Naoki
Akama, Kazuhito
Matsumoto, Ken-Ichi
author_sort Yamaguchi, Shinsaku
collection PubMed
description Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In the present study, the contribution of TNX to liver dysfunction was investigated by administration of high-fat and high-cholesterol diet with high levels of phosphorus and calcium (HFCD) to wild-type (WT) and TNX-knockout (KO) mice. After 16 weeks of HFCD administration, the ratio of liver weight to body weight was approximately 22% higher in the HFCD-fed WT mice compared with the HFCD-fed TNX-KO mice, indicating hepatomegaly in HFCD-fed WT mice. Histological analyses with hematoxylin and eosin staining at 21 weeks revealed that hepatocyte hypertrophy in HFCD-fed TNX-KO mice was suppressed to 85% of that in HFCD-fed WT mice. By contrast, there was a 1.2-fold increase in lipid deposition in hepatocytes from HFCD-fed TNX-KO mice compared with HFCD-fed WT mice at 18 weeks, as demonstrated by Oil Red O staining. In addition, TNX-KO mice at 21 weeks and 27 weeks post-HFCD administration exhibited significant suppression of inflammatory cell infiltrate to 51 and 24% of that in WT mice, respectively. Immunofluorescence analysis for type I collagen and Elastica van Gieson staining demonstrated a clear hepatic fibrosis progression in HFCD-fed WT mice at 27 weeks, whereas hepatic fibrosis was undetected in HFCD-fed TNX-KO mice. The present findings indicated that TNX deficiency suppressed hepatic dysfunction induced by HFCD administration.
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spelling pubmed-56469882017-10-24 Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet Yamaguchi, Shinsaku Kawakami, Kohei Satoh, Kazumi Fukunaga, Naoki Akama, Kazuhito Matsumoto, Ken-Ichi Mol Med Rep Articles Extracellular matrix glycoprotein tenascin-X (TNX) is the largest member of the tenascin family. In the present study, the contribution of TNX to liver dysfunction was investigated by administration of high-fat and high-cholesterol diet with high levels of phosphorus and calcium (HFCD) to wild-type (WT) and TNX-knockout (KO) mice. After 16 weeks of HFCD administration, the ratio of liver weight to body weight was approximately 22% higher in the HFCD-fed WT mice compared with the HFCD-fed TNX-KO mice, indicating hepatomegaly in HFCD-fed WT mice. Histological analyses with hematoxylin and eosin staining at 21 weeks revealed that hepatocyte hypertrophy in HFCD-fed TNX-KO mice was suppressed to 85% of that in HFCD-fed WT mice. By contrast, there was a 1.2-fold increase in lipid deposition in hepatocytes from HFCD-fed TNX-KO mice compared with HFCD-fed WT mice at 18 weeks, as demonstrated by Oil Red O staining. In addition, TNX-KO mice at 21 weeks and 27 weeks post-HFCD administration exhibited significant suppression of inflammatory cell infiltrate to 51 and 24% of that in WT mice, respectively. Immunofluorescence analysis for type I collagen and Elastica van Gieson staining demonstrated a clear hepatic fibrosis progression in HFCD-fed WT mice at 27 weeks, whereas hepatic fibrosis was undetected in HFCD-fed TNX-KO mice. The present findings indicated that TNX deficiency suppressed hepatic dysfunction induced by HFCD administration. D.A. Spandidos 2017-10 2017-07-21 /pmc/articles/PMC5646988/ /pubmed/28731143 http://dx.doi.org/10.3892/mmr.2017.7052 Text en Copyright: © Yamaguchi et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Yamaguchi, Shinsaku
Kawakami, Kohei
Satoh, Kazumi
Fukunaga, Naoki
Akama, Kazuhito
Matsumoto, Ken-Ichi
Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title_full Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title_fullStr Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title_full_unstemmed Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title_short Suppression of hepatic dysfunction in tenascin-X-deficient mice fed a high-fat diet
title_sort suppression of hepatic dysfunction in tenascin-x-deficient mice fed a high-fat diet
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5646988/
https://www.ncbi.nlm.nih.gov/pubmed/28731143
http://dx.doi.org/10.3892/mmr.2017.7052
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