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PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism
Peroxisome proliferator activated receptor gamma 2 (PPARg2) is the nutritionally regulated isoform of PPARg. Ablation of PPARg2 in the ob/ob background, PPARg2(−/−) Lep(ob)/Lep(ob) (POKO mouse), resulted in decreased fat mass, severe insulin resistance, β-cell failure, and dyslipidaemia. Our results...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Public Library of Science
2007
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857730/ https://www.ncbi.nlm.nih.gov/pubmed/17465682 http://dx.doi.org/10.1371/journal.pgen.0030064 |
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author | Medina-Gomez, Gema Gray, Sarah L Yetukuri, Laxman Shimomura, Kenju Virtue, Sam Campbell, Mark Curtis, R. Keira Jimenez-Linan, Mercedes Blount, Margaret Yeo, Giles S. H Lopez, Miguel Seppänen-Laakso, Tuulikki Ashcroft, Frances M Orešič, Matej Vidal-Puig, Antonio |
author_facet | Medina-Gomez, Gema Gray, Sarah L Yetukuri, Laxman Shimomura, Kenju Virtue, Sam Campbell, Mark Curtis, R. Keira Jimenez-Linan, Mercedes Blount, Margaret Yeo, Giles S. H Lopez, Miguel Seppänen-Laakso, Tuulikki Ashcroft, Frances M Orešič, Matej Vidal-Puig, Antonio |
author_sort | Medina-Gomez, Gema |
collection | PubMed |
description | Peroxisome proliferator activated receptor gamma 2 (PPARg2) is the nutritionally regulated isoform of PPARg. Ablation of PPARg2 in the ob/ob background, PPARg2(−/−) Lep(ob)/Lep(ob) (POKO mouse), resulted in decreased fat mass, severe insulin resistance, β-cell failure, and dyslipidaemia. Our results indicate that the PPARg2 isoform plays an important role, mediating adipose tissue expansion in response to positive energy balance. Lipidomic analyses suggest that PPARg2 plays an important antilipotoxic role when induced ectopically in liver and muscle by facilitating deposition of fat as relatively harmless triacylglycerol species and thus preventing accumulation of reactive lipid species. Our data also indicate that PPARg2 may be required for the β-cell hypertrophic adaptive response to insulin resistance. In summary, the PPARg2 isoform prevents lipotoxicity by (a) promoting adipose tissue expansion, (b) increasing the lipid-buffering capacity of peripheral organs, and (c) facilitating the adaptive proliferative response of β-cells to insulin resistance. |
format | Text |
id | pubmed-1857730 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-18577302007-04-27 PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism Medina-Gomez, Gema Gray, Sarah L Yetukuri, Laxman Shimomura, Kenju Virtue, Sam Campbell, Mark Curtis, R. Keira Jimenez-Linan, Mercedes Blount, Margaret Yeo, Giles S. H Lopez, Miguel Seppänen-Laakso, Tuulikki Ashcroft, Frances M Orešič, Matej Vidal-Puig, Antonio PLoS Genet Research Article Peroxisome proliferator activated receptor gamma 2 (PPARg2) is the nutritionally regulated isoform of PPARg. Ablation of PPARg2 in the ob/ob background, PPARg2(−/−) Lep(ob)/Lep(ob) (POKO mouse), resulted in decreased fat mass, severe insulin resistance, β-cell failure, and dyslipidaemia. Our results indicate that the PPARg2 isoform plays an important role, mediating adipose tissue expansion in response to positive energy balance. Lipidomic analyses suggest that PPARg2 plays an important antilipotoxic role when induced ectopically in liver and muscle by facilitating deposition of fat as relatively harmless triacylglycerol species and thus preventing accumulation of reactive lipid species. Our data also indicate that PPARg2 may be required for the β-cell hypertrophic adaptive response to insulin resistance. In summary, the PPARg2 isoform prevents lipotoxicity by (a) promoting adipose tissue expansion, (b) increasing the lipid-buffering capacity of peripheral organs, and (c) facilitating the adaptive proliferative response of β-cells to insulin resistance. Public Library of Science 2007-04 2007-04-27 /pmc/articles/PMC1857730/ /pubmed/17465682 http://dx.doi.org/10.1371/journal.pgen.0030064 Text en © 2007 Medina-Gomez et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Medina-Gomez, Gema Gray, Sarah L Yetukuri, Laxman Shimomura, Kenju Virtue, Sam Campbell, Mark Curtis, R. Keira Jimenez-Linan, Mercedes Blount, Margaret Yeo, Giles S. H Lopez, Miguel Seppänen-Laakso, Tuulikki Ashcroft, Frances M Orešič, Matej Vidal-Puig, Antonio PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title | PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title_full | PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title_fullStr | PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title_full_unstemmed | PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title_short | PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism |
title_sort | ppar gamma 2 prevents lipotoxicity by controlling adipose tissue expandability and peripheral lipid metabolism |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857730/ https://www.ncbi.nlm.nih.gov/pubmed/17465682 http://dx.doi.org/10.1371/journal.pgen.0030064 |
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