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Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease

We previously demonstrated that a common dietary protein component, wheat amylase trypsin inhibitors (ATI), stimulate intestinal macrophages and dendritic cells via toll like receptor 4. Activation of these intestinal myeloid cells elicits an inflammatory signal that is propagated to mesenteric lymp...

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Autores principales: Ashfaq-Khan, Muhammad, Aslam, Misbah, Qureshi, Muhammad Asif, Senkowski, Marcel Sascha, Yen-Weng, Shih, Strand, Susanne, Kim, Yong Ook, Pickert, Geethanjali, Schattenberg, Jörn M., Schuppan, Detlef
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877510/
https://www.ncbi.nlm.nih.gov/pubmed/31767938
http://dx.doi.org/10.1038/s41598-019-53323-x
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author Ashfaq-Khan, Muhammad
Aslam, Misbah
Qureshi, Muhammad Asif
Senkowski, Marcel Sascha
Yen-Weng, Shih
Strand, Susanne
Kim, Yong Ook
Pickert, Geethanjali
Schattenberg, Jörn M.
Schuppan, Detlef
author_facet Ashfaq-Khan, Muhammad
Aslam, Misbah
Qureshi, Muhammad Asif
Senkowski, Marcel Sascha
Yen-Weng, Shih
Strand, Susanne
Kim, Yong Ook
Pickert, Geethanjali
Schattenberg, Jörn M.
Schuppan, Detlef
author_sort Ashfaq-Khan, Muhammad
collection PubMed
description We previously demonstrated that a common dietary protein component, wheat amylase trypsin inhibitors (ATI), stimulate intestinal macrophages and dendritic cells via toll like receptor 4. Activation of these intestinal myeloid cells elicits an inflammatory signal that is propagated to mesenteric lymph nodes, and that can facilitate extraintestinal inflammation. Mice were fed a well-defined high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amounts of ATI. Mice on HFD/ATI developed only mild signs of intestinal inflammation and myeloid cell activation but displayed significantly higher serum triglycerides and transaminases compared to mice on HFD alone. Moreover, they showed increased visceral and liver fat, and a higher insulin resistance. ATI feeding promoted liver and adipose tissue inflammation, with M1-type macrophage polarization and infiltration, and enhanced liver fibrogenesis. Gluten, the major protein component of wheat, did not induce these pathologies. Therefore, wheat ATI ingestion in minute quantities comparable to human daily wheat consumption exacerbated features of the metabolic syndrome and non-alcoholic steatohepatitis, despite its irrelevant caloric value.
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spelling pubmed-68775102019-12-05 Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease Ashfaq-Khan, Muhammad Aslam, Misbah Qureshi, Muhammad Asif Senkowski, Marcel Sascha Yen-Weng, Shih Strand, Susanne Kim, Yong Ook Pickert, Geethanjali Schattenberg, Jörn M. Schuppan, Detlef Sci Rep Article We previously demonstrated that a common dietary protein component, wheat amylase trypsin inhibitors (ATI), stimulate intestinal macrophages and dendritic cells via toll like receptor 4. Activation of these intestinal myeloid cells elicits an inflammatory signal that is propagated to mesenteric lymph nodes, and that can facilitate extraintestinal inflammation. Mice were fed a well-defined high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amounts of ATI. Mice on HFD/ATI developed only mild signs of intestinal inflammation and myeloid cell activation but displayed significantly higher serum triglycerides and transaminases compared to mice on HFD alone. Moreover, they showed increased visceral and liver fat, and a higher insulin resistance. ATI feeding promoted liver and adipose tissue inflammation, with M1-type macrophage polarization and infiltration, and enhanced liver fibrogenesis. Gluten, the major protein component of wheat, did not induce these pathologies. Therefore, wheat ATI ingestion in minute quantities comparable to human daily wheat consumption exacerbated features of the metabolic syndrome and non-alcoholic steatohepatitis, despite its irrelevant caloric value. Nature Publishing Group UK 2019-11-25 /pmc/articles/PMC6877510/ /pubmed/31767938 http://dx.doi.org/10.1038/s41598-019-53323-x Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Ashfaq-Khan, Muhammad
Aslam, Misbah
Qureshi, Muhammad Asif
Senkowski, Marcel Sascha
Yen-Weng, Shih
Strand, Susanne
Kim, Yong Ook
Pickert, Geethanjali
Schattenberg, Jörn M.
Schuppan, Detlef
Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title_full Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title_fullStr Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title_full_unstemmed Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title_short Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
title_sort dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877510/
https://www.ncbi.nlm.nih.gov/pubmed/31767938
http://dx.doi.org/10.1038/s41598-019-53323-x
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