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Int. J. Mol. Sci. 2016, 17(8), 1236; doi:10.3390/ijms17081236

Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases?

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary
Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, FL 32877, USA
MTA-DE “Lendulet” Immunogenomics Research Group, University of Debrecen, Debrecen H-4012, Hungary
Author to whom correspondence should be addressed.
Academic Editor: Béatrice Desvergne
Received: 22 June 2016 / Revised: 19 July 2016 / Accepted: 21 July 2016 / Published: 30 July 2016
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With the increasing number of patients affected with metabolic diseases such as type 2 diabetes, obesity, atherosclerosis and insulin resistance, academic researchers and pharmaceutical companies are eager to better understand metabolic syndrome and develop new drugs for its treatment. Many studies have focused on the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), which plays a crucial role in adipogenesis and lipid metabolism. These studies have been able to connect this transcription factor to several human metabolic diseases. Due to obvious limitations concerning experimentation in humans, animal models—mainly mouse models—have been generated to investigate the role of PPARγ in different tissues. This review focuses on the metabolic features of human and mouse PPARγ-related diseases and the utility of the mouse as a model. View Full-Text
Keywords: PPARγ expression; human mutations; mouse models; metabolic syndrome; lipodystrophy; ligand activation PPARγ expression; human mutations; mouse models; metabolic syndrome; lipodystrophy; ligand activation

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. (CC BY 4.0).

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Pap, A.; Cuaranta-Monroy, I.; Peloquin, M.; Nagy, L. Is the Mouse a Good Model of Human PPARγ-Related Metabolic Diseases? Int. J. Mol. Sci. 2016, 17, 1236.

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