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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...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
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.
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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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