PPARs in Calorie Restricted and Genetically Long-Lived Mice

doi:10.1155/2007/28436

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PPAR Research
Volume 2007 (2007), Article ID 28436, 7 pages
doi:10.1155/2007/28436

Review Article

PPARs in Calorie Restricted and Genetically Long-Lived Mice

Michal M. Masternak¹ and Andrzej Bartke^1,2

¹Departments of Internal Medicine, Geriatrics Research, School of Medicine, Southern Illinois University, Springfield 62794, IL, USA
²Departments of Physiology, Geriatrics Research, School of Medicine, Southern Illinois University, Springfield 62794, IL, USA

Received 15 August 2006; Revised 18 October 2006; Accepted 18 October 2006

Academic Editor: Francine M. Gregoire

Copyright © 2007 Michal M. Masternak and Andrzej Bartke. 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.

Abstract

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.