TY - JOUR
T1 - PPARγ in human and mouse physiology
AU - Heikkinen, Sami
AU - Auwerx, Johan
AU - Argmann, Carmen A.
N1 - Funding Information:
This work was supported by grants from CNRS, INSERM, Hopitaux Universitaires de Strasbourg, Academy of Finland, EU, EMBO and NIH (DK67320). We thank the members of the Auwerx Laboratory for helpful discussions.
PY - 2007/8
Y1 - 2007/8
N2 - The peroxisome proliferator activated receptor gamma (PPARγ) is a member in the nuclear receptor superfamily which mediates part of the regulatory effects of dietary fatty acids on gene expression. As PPARγ also coordinates adipocyte differentiation, it is an important component in storing the excess nutritional energy as fat. Our genes have evolved into maximizing energy storage, and PPARγ has a central role in the mismatch between our genes and our affluent western society which results in a broad range of metabolic disturbances, collectively known as the metabolic syndrome. A flurry of human and mouse studies has shed new light on the mechanisms how the commonly used insulin sensitizer drugs and PPARγ activators, thiazolidinediones, act, and which of their physiological effects are dependent of PPARγ. It is now evident that the full activation of PPARγ is less advantageous than targeted modulation of its activity. Furthermore, new roles for PPARγ signaling have been discovered in inflammation, bone morphogenesis, endothelial function, cancer, longevity, and atherosclerosis, to mention a few. Here we draw together and discuss these recent advances in the research into PPARγ biology.
AB - The peroxisome proliferator activated receptor gamma (PPARγ) is a member in the nuclear receptor superfamily which mediates part of the regulatory effects of dietary fatty acids on gene expression. As PPARγ also coordinates adipocyte differentiation, it is an important component in storing the excess nutritional energy as fat. Our genes have evolved into maximizing energy storage, and PPARγ has a central role in the mismatch between our genes and our affluent western society which results in a broad range of metabolic disturbances, collectively known as the metabolic syndrome. A flurry of human and mouse studies has shed new light on the mechanisms how the commonly used insulin sensitizer drugs and PPARγ activators, thiazolidinediones, act, and which of their physiological effects are dependent of PPARγ. It is now evident that the full activation of PPARγ is less advantageous than targeted modulation of its activity. Furthermore, new roles for PPARγ signaling have been discovered in inflammation, bone morphogenesis, endothelial function, cancer, longevity, and atherosclerosis, to mention a few. Here we draw together and discuss these recent advances in the research into PPARγ biology.
KW - Bone homeostasis
KW - Human genetic variants
KW - Longevity
KW - Metabolism
KW - Mouse models
KW - PPARγ
UR - http://www.scopus.com/inward/record.url?scp=34547565190&partnerID=8YFLogxK
U2 - 10.1016/j.bbalip.2007.03.006
DO - 10.1016/j.bbalip.2007.03.006
M3 - Review article
C2 - 17475546
AN - SCOPUS:34547565190
SN - 1388-1981
VL - 1771
SP - 999
EP - 1013
JO - Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
JF - Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
IS - 8
ER -