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Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice
WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Lepr...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666495/ https://www.ncbi.nlm.nih.gov/pubmed/33292732 http://dx.doi.org/10.1186/s42826-020-00076-8 |
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author | Mishra, Arun Prakash Siva, Archana B. Gurunathan, Chandrashekaran Komala, Y. Lakshmi, B. Jyothi |
author_facet | Mishra, Arun Prakash Siva, Archana B. Gurunathan, Chandrashekaran Komala, Y. Lakshmi, B. Jyothi |
author_sort | Mishra, Arun Prakash |
collection | PubMed |
description | WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Lepr(db/db) mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13(−/0) mice using hepatotoxin CCl(4). In the present study we report slower hepatic regeneration in Wdr13(−/0) mice as compared to their wild type littermates after CCl(4) administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13(−/0) mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl(4)- administered Wdr13(−/0) mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl(4) administered Wdr13(−/0) mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42826-020-00076-8. |
format | Online Article Text |
id | pubmed-7666495 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-76664952020-11-16 Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice Mishra, Arun Prakash Siva, Archana B. Gurunathan, Chandrashekaran Komala, Y. Lakshmi, B. Jyothi Lab Anim Res Research WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Lepr(db/db) mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13(−/0) mice using hepatotoxin CCl(4). In the present study we report slower hepatic regeneration in Wdr13(−/0) mice as compared to their wild type littermates after CCl(4) administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13(−/0) mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl(4)- administered Wdr13(−/0) mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl(4) administered Wdr13(−/0) mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42826-020-00076-8. BioMed Central 2020-11-13 /pmc/articles/PMC7666495/ /pubmed/33292732 http://dx.doi.org/10.1186/s42826-020-00076-8 Text en © The Author(s) 2020 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Mishra, Arun Prakash Siva, Archana B. Gurunathan, Chandrashekaran Komala, Y. Lakshmi, B. Jyothi Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title | Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title_full | Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title_fullStr | Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title_full_unstemmed | Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title_short | Impaired liver regeneration and lipid homeostasis in CCl(4) treated WDR13 deficient mice |
title_sort | impaired liver regeneration and lipid homeostasis in ccl(4) treated wdr13 deficient mice |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7666495/ https://www.ncbi.nlm.nih.gov/pubmed/33292732 http://dx.doi.org/10.1186/s42826-020-00076-8 |
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