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p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.

BCL-2 proteins have been implicated in the control of glucose homeostasis and metabolism in different cell types. Thus, the aim of this study was to determine the role of the pro-apoptotic BH3-only protein, p53-upregulated-modulator-of-apoptosis (PUMA), in metabolic changes mediated by diet-induced...

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Autores principales: Litwak, Sara A., Loh, Kim, Stanley, William J., Pappas, Evan G., Wali, Jibran A., Selck, Claudia, Strasser, Andreas, Thomas, Helen E., Gurzov, Esteban N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817123/
https://www.ncbi.nlm.nih.gov/pubmed/27033313
http://dx.doi.org/10.1038/srep23802
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author Litwak, Sara A.
Loh, Kim
Stanley, William J.
Pappas, Evan G.
Wali, Jibran A.
Selck, Claudia
Strasser, Andreas
Thomas, Helen E.
Gurzov, Esteban N.
author_facet Litwak, Sara A.
Loh, Kim
Stanley, William J.
Pappas, Evan G.
Wali, Jibran A.
Selck, Claudia
Strasser, Andreas
Thomas, Helen E.
Gurzov, Esteban N.
author_sort Litwak, Sara A.
collection PubMed
description BCL-2 proteins have been implicated in the control of glucose homeostasis and metabolism in different cell types. Thus, the aim of this study was to determine the role of the pro-apoptotic BH3-only protein, p53-upregulated-modulator-of-apoptosis (PUMA), in metabolic changes mediated by diet-induced obesity, using PUMA deficient mice. At 10 weeks of age, knockout and wild type mice either continued consuming a low fat chow diet (6% fat), or were fed with a high fat diet (23% fat) for 14–17 weeks. We measured body composition, glucose and insulin tolerance, insulin response in peripheral tissues, energy expenditure, oxygen consumption, and respiratory exchange ratio in vivo. All these parameters were indistinguishable between wild type and knockout mice on chow diet and were modified equally by diet-induced obesity. Interestingly, we observed decreased food intake and ambulatory capacity of PUMA knockout mice on high fat diet. This was associated with increased adipocyte size and fasted leptin concentration in the blood. Our findings suggest that although PUMA is dispensable for glucose homeostasis in lean and obese mice, it can affect leptin levels and food intake during obesity.
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spelling pubmed-48171232016-04-05 p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity. Litwak, Sara A. Loh, Kim Stanley, William J. Pappas, Evan G. Wali, Jibran A. Selck, Claudia Strasser, Andreas Thomas, Helen E. Gurzov, Esteban N. Sci Rep Article BCL-2 proteins have been implicated in the control of glucose homeostasis and metabolism in different cell types. Thus, the aim of this study was to determine the role of the pro-apoptotic BH3-only protein, p53-upregulated-modulator-of-apoptosis (PUMA), in metabolic changes mediated by diet-induced obesity, using PUMA deficient mice. At 10 weeks of age, knockout and wild type mice either continued consuming a low fat chow diet (6% fat), or were fed with a high fat diet (23% fat) for 14–17 weeks. We measured body composition, glucose and insulin tolerance, insulin response in peripheral tissues, energy expenditure, oxygen consumption, and respiratory exchange ratio in vivo. All these parameters were indistinguishable between wild type and knockout mice on chow diet and were modified equally by diet-induced obesity. Interestingly, we observed decreased food intake and ambulatory capacity of PUMA knockout mice on high fat diet. This was associated with increased adipocyte size and fasted leptin concentration in the blood. Our findings suggest that although PUMA is dispensable for glucose homeostasis in lean and obese mice, it can affect leptin levels and food intake during obesity. Nature Publishing Group 2016-04-01 /pmc/articles/PMC4817123/ /pubmed/27033313 http://dx.doi.org/10.1038/srep23802 Text en Copyright © 2016, Macmillan Publishers Limited 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
Litwak, Sara A.
Loh, Kim
Stanley, William J.
Pappas, Evan G.
Wali, Jibran A.
Selck, Claudia
Strasser, Andreas
Thomas, Helen E.
Gurzov, Esteban N.
p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title_full p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title_fullStr p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title_full_unstemmed p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title_short p53-upregulated-modulator-of-apoptosis (PUMA) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
title_sort p53-upregulated-modulator-of-apoptosis (puma) deficiency affects food intake but does not impact on body weight or glucose homeostasis in diet-induced obesity.
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817123/
https://www.ncbi.nlm.nih.gov/pubmed/27033313
http://dx.doi.org/10.1038/srep23802
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