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Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications
Several studies in the past have reported positive correlations between circulating Serum amyloid A (SAA) levels and obesity. However, based on limited number of studies involving appropriate mouse models, the role of SAA in the development of obesity and obesity-related metabolic consequences has n...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9015120/ https://www.ncbi.nlm.nih.gov/pubmed/35436297 http://dx.doi.org/10.1371/journal.pone.0266688 |
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author | Ji, Ailing Trumbauer, Andrea C. Noffsinger, Victoria P. Jeon, Hayce Patrick, Avery C. De Beer, Frederick C. Webb, Nancy R. Tannock, Lisa R. Shridas, Preetha |
author_facet | Ji, Ailing Trumbauer, Andrea C. Noffsinger, Victoria P. Jeon, Hayce Patrick, Avery C. De Beer, Frederick C. Webb, Nancy R. Tannock, Lisa R. Shridas, Preetha |
author_sort | Ji, Ailing |
collection | PubMed |
description | Several studies in the past have reported positive correlations between circulating Serum amyloid A (SAA) levels and obesity. However, based on limited number of studies involving appropriate mouse models, the role of SAA in the development of obesity and obesity-related metabolic consequences has not been established. Accordingly, herein, we have examined the role of SAA in the development of obesity and its associated metabolic complications in vivo using mice deficient for all three inducible forms of SAA: SAA1.1, SAA2.1 and SAA3 (TKO). Male and female mice were rendered obese by feeding a high fat, high sucrose diet with added cholesterol (HFHSC) and control mice were fed rodent chow diet. Here, we show that the deletion of SAA does not affect diet-induced obesity, hepatic lipid metabolism or adipose tissue inflammation. However, there was a modest effect on glucose metabolism. The results of this study confirm previous findings that SAA levels are elevated in adipose tissues as well as in the circulation in diet-induced obese mice. However, the three acute phase SAAs do not play a causative role in the development of obesity or obesity-associated adipose tissue inflammation and dyslipidemia. |
format | Online Article Text |
id | pubmed-9015120 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-90151202022-04-19 Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications Ji, Ailing Trumbauer, Andrea C. Noffsinger, Victoria P. Jeon, Hayce Patrick, Avery C. De Beer, Frederick C. Webb, Nancy R. Tannock, Lisa R. Shridas, Preetha PLoS One Research Article Several studies in the past have reported positive correlations between circulating Serum amyloid A (SAA) levels and obesity. However, based on limited number of studies involving appropriate mouse models, the role of SAA in the development of obesity and obesity-related metabolic consequences has not been established. Accordingly, herein, we have examined the role of SAA in the development of obesity and its associated metabolic complications in vivo using mice deficient for all three inducible forms of SAA: SAA1.1, SAA2.1 and SAA3 (TKO). Male and female mice were rendered obese by feeding a high fat, high sucrose diet with added cholesterol (HFHSC) and control mice were fed rodent chow diet. Here, we show that the deletion of SAA does not affect diet-induced obesity, hepatic lipid metabolism or adipose tissue inflammation. However, there was a modest effect on glucose metabolism. The results of this study confirm previous findings that SAA levels are elevated in adipose tissues as well as in the circulation in diet-induced obese mice. However, the three acute phase SAAs do not play a causative role in the development of obesity or obesity-associated adipose tissue inflammation and dyslipidemia. Public Library of Science 2022-04-18 /pmc/articles/PMC9015120/ /pubmed/35436297 http://dx.doi.org/10.1371/journal.pone.0266688 Text en © 2022 Ji et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Ji, Ailing Trumbauer, Andrea C. Noffsinger, Victoria P. Jeon, Hayce Patrick, Avery C. De Beer, Frederick C. Webb, Nancy R. Tannock, Lisa R. Shridas, Preetha Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title | Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title_full | Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title_fullStr | Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title_full_unstemmed | Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title_short | Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
title_sort | serum amyloid a is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9015120/ https://www.ncbi.nlm.nih.gov/pubmed/35436297 http://dx.doi.org/10.1371/journal.pone.0266688 |
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