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PPARs in Calorie Restricted and Genetically Long-Lived Mice

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptors superfamily. The three subtypes, PPARα, PPARγ, and PPARβ/δ, are expressed in multiple organs. These transcription factors regulate different physiological functions such as energy metabolism (including lipid and...

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Detalles Bibliográficos
Autores principales: Masternak, Michal M., Bartke, Andrzej
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779582/
https://www.ncbi.nlm.nih.gov/pubmed/17389764
http://dx.doi.org/10.1155/2007/28436
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author Masternak, Michal M.
Bartke, Andrzej
author_facet Masternak, Michal M.
Bartke, Andrzej
author_sort Masternak, Michal M.
collection PubMed
description Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptors superfamily. The three subtypes, PPARα, PPARγ, and PPARβ/δ, are expressed in multiple organs. These transcription factors regulate different physiological functions such as energy metabolism (including lipid and carbohydrate metabolism), insulin action, and immunity and inflammation, and apparently also act as important mediators of longevity and aging. Calorie restriction (CR) is the most effective intervention known to delay aging and increase lifespan. Calorie restriction affects the same physiological functions as PPARs. This review summarizes recent findings on the effects of CR and aging on the expression of PPARγ, α, and β/δ in mice and discusses possible involvement of PPARs in mediating the effects of murine longevity genes. The levels of PPARs change with age and CR appears to prevent these alterations which make “PPARs-CR-AGING” dependence of considerable interest.
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spelling pubmed-17795822007-02-01 PPARs in Calorie Restricted and Genetically Long-Lived Mice Masternak, Michal M. Bartke, Andrzej PPAR Res Review Article Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptors superfamily. The three subtypes, PPARα, PPARγ, and PPARβ/δ, are expressed in multiple organs. These transcription factors regulate different physiological functions such as energy metabolism (including lipid and carbohydrate metabolism), insulin action, and immunity and inflammation, and apparently also act as important mediators of longevity and aging. Calorie restriction (CR) is the most effective intervention known to delay aging and increase lifespan. Calorie restriction affects the same physiological functions as PPARs. This review summarizes recent findings on the effects of CR and aging on the expression of PPARγ, α, and β/δ in mice and discusses possible involvement of PPARs in mediating the effects of murine longevity genes. The levels of PPARs change with age and CR appears to prevent these alterations which make “PPARs-CR-AGING” dependence of considerable interest. Hindawi Publishing Corporation 2007 2006-11-28 /pmc/articles/PMC1779582/ /pubmed/17389764 http://dx.doi.org/10.1155/2007/28436 Text en Copyright © 2007 M. M. Masternak and A. Bartke https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Masternak, Michal M.
Bartke, Andrzej
PPARs in Calorie Restricted and Genetically Long-Lived Mice
title PPARs in Calorie Restricted and Genetically Long-Lived Mice
title_full PPARs in Calorie Restricted and Genetically Long-Lived Mice
title_fullStr PPARs in Calorie Restricted and Genetically Long-Lived Mice
title_full_unstemmed PPARs in Calorie Restricted and Genetically Long-Lived Mice
title_short PPARs in Calorie Restricted and Genetically Long-Lived Mice
title_sort ppars in calorie restricted and genetically long-lived mice
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779582/
https://www.ncbi.nlm.nih.gov/pubmed/17389764
http://dx.doi.org/10.1155/2007/28436
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