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Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet
F13A1 gene, which encodes for Factor XIII-A blood clotting factor and a transglutaminase enzyme, was recently identified as a potential causative gene for obesity in humans. In our previous in vitro work, we showed that FXIII-A regulates preadipocyte differentiation and modulates insulin signaling v...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5069677/ https://www.ncbi.nlm.nih.gov/pubmed/27759118 http://dx.doi.org/10.1038/srep35574 |
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author | Myneni, Vamsee D. Mousa, Aisha Kaartinen, Mari T. |
author_facet | Myneni, Vamsee D. Mousa, Aisha Kaartinen, Mari T. |
author_sort | Myneni, Vamsee D. |
collection | PubMed |
description | F13A1 gene, which encodes for Factor XIII-A blood clotting factor and a transglutaminase enzyme, was recently identified as a potential causative gene for obesity in humans. In our previous in vitro work, we showed that FXIII-A regulates preadipocyte differentiation and modulates insulin signaling via promoting plasma fibronectin assembly into the extracellular matrix. To understand the role of FXIII-A in whole body energy metabolism, here we have characterized the metabolic phenotype of F13a1−/− mice. F13a1−/− and F13a1+/+ type mice were fed chow or obesogenic, high fat diet for 20 weeks. Weight gain, total fat mass and fat pad mass, glucose handling, insulin sensitivity, energy expenditure and, morphological and biochemical analysis of adipose tissue was performed. We show that mice lacking FXIII-A gain weight on obesogenic diet, similarly as wild type mice, but exhibit a number of features of metabolically healthy obesity such as protection from developing diet-induced insulin resistance and hyperinsulinemia. Mice also show normal fasting glucose levels, larger adipocytes, decreased extracellular matrix accumulation and inflammation of adipose tissue, as well as decreased circulating triglycerides. This study reveals that FXIII-A transglutaminase can regulate whole body insulin sensitivity and may have a role in the development of diet-induced metabolic disturbances. |
format | Online Article Text |
id | pubmed-5069677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-50696772016-10-26 Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet Myneni, Vamsee D. Mousa, Aisha Kaartinen, Mari T. Sci Rep Article F13A1 gene, which encodes for Factor XIII-A blood clotting factor and a transglutaminase enzyme, was recently identified as a potential causative gene for obesity in humans. In our previous in vitro work, we showed that FXIII-A regulates preadipocyte differentiation and modulates insulin signaling via promoting plasma fibronectin assembly into the extracellular matrix. To understand the role of FXIII-A in whole body energy metabolism, here we have characterized the metabolic phenotype of F13a1−/− mice. F13a1−/− and F13a1+/+ type mice were fed chow or obesogenic, high fat diet for 20 weeks. Weight gain, total fat mass and fat pad mass, glucose handling, insulin sensitivity, energy expenditure and, morphological and biochemical analysis of adipose tissue was performed. We show that mice lacking FXIII-A gain weight on obesogenic diet, similarly as wild type mice, but exhibit a number of features of metabolically healthy obesity such as protection from developing diet-induced insulin resistance and hyperinsulinemia. Mice also show normal fasting glucose levels, larger adipocytes, decreased extracellular matrix accumulation and inflammation of adipose tissue, as well as decreased circulating triglycerides. This study reveals that FXIII-A transglutaminase can regulate whole body insulin sensitivity and may have a role in the development of diet-induced metabolic disturbances. Nature Publishing Group 2016-10-19 /pmc/articles/PMC5069677/ /pubmed/27759118 http://dx.doi.org/10.1038/srep35574 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Myneni, Vamsee D. Mousa, Aisha Kaartinen, Mari T. Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title | Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title_full | Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title_fullStr | Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title_full_unstemmed | Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title_short | Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
title_sort | factor xiii-a transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5069677/ https://www.ncbi.nlm.nih.gov/pubmed/27759118 http://dx.doi.org/10.1038/srep35574 |
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