PPARγ, the ultimate thrifty gene

Auwerx, J.

doi:10.1007/s001250051268

Cited by 612Peroxisome Proliferator-Activated ReceptorsAdipose Tissue and MetabolismAdipokines, Inflammation, and Metabolic Diseases

PPARγ, the ultimate thrifty gene

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Auwerx, J.·1999·Diabetologia

DOI 10.1007/s001250051268

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Abstract

The peroxisome proliferator-activated receptor gamma (PPARgamma) quickly evolved over the last decade from a new orphan receptor to one of the best characterized nuclear receptors. This fast pace in PPARgamma research was triggered by two main discoveries. Firstly, that PPARgamma was shown to have a key role in adipogenesis and be a master controller of the "thrifty gene response" leading to efficient energy storage. Secondly, the discovery that its synthetic ligands, the thiazolidinediones, are promising insulin sensitizing drugs, which are currently being developed for the treatment of Type II (non-insulin-dependent) diabetes mellitus. More recently this nuclear receptor emerged from a role limited to metabolism (diabetes and obesity) to a power player in general transcriptional control of numerous cellular processes, with implications in cell cycle control, carcinogenesis, inflammation, atherosclerosis and immunomodulation. This widened role of PPARgamma will certainly initiate a new flurry of research, which will not only refine our current often partial knowledge of PPARgamma but more importantly also establish that this receptor has a definite role as a primary link adapting cellular, tissue and whole body homeostasis to energy stores.

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Thiazolidinediones, which induce adipocyte differentiation, improve insulin sensitivity and increase fat deposition in the subcutaneous rather than the intra-abdominal fat compartment.
“the thiazolidinediones, which induce adipocyte differentiation [63], not only improve insulin sensitivity but also increase fat deposition in the subcutaneous rather than the intra-abdominal fat compartment [64, 65].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [63]

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Authors: Auwerx, J.
Affiliations: Institut Pasteur de Lille (FR)
Corresponding author: Auwerx, J.
ORCID: Auwerx, J.
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 1999-08-19
Volume: 42
Issue: 9
Pages: 1033-1049
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s001250051268
OpenAlex: W91098912
Cited by: 612
References: 100
Citations by year: 2026: 2 · 2025: 4 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 10 · 2020: 3 · 2019: 5 · 2018: 14 · 2017: 8 · 2016: 20 · 2015: 13 · 2014: 17 · 2013: 22 · 2012: 17
FWCI: 15.76
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Diabetologia (publishedVersion)
PubMed (publishedVersion)
Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords: PPARγ, nuclear receptors, orphan receptors, adipogenesis, energy storage, thiazolidinediones, insulin sensitizers, type 2 diabetes, obesity, transcriptional regulation, cell cycle regulation, carcinogenesis, inflammation, atherosclerosis, immunomodulation, homeostasis
MeSH terms: Adipose Tissue, Animals, Cell Cycle, Diabetes Mellitus, Type 2, Energy Metabolism, Humans, Insulin, Microbodies, Obesity, Transcription Factors, Receptors, Cytoplasmic and Nuclear

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