PPARs: diverse regulators in energy metabolism and metabolic diseases
Open accessAbstract
The nuclear receptor PPARs are fundamentally important for energy homeostasis. Through their distinct yet overlapping functions and tissue distribution, the PPARs regulate many aspects of energy metabolism at the transcriptional level. Functional impairment or dysregulation of these receptors leads to a variety of metabolic diseases, while their ligands offer many metabolic benefits. Studies of these receptors have advanced our knowledge of the transcriptional basis of energy metabolism and helped us understand the pathogenic mechanisms of metabolic syndrome.
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GW9662 influences genes in all classic PPAR-related metabolic pathways (lipid metabolism, glucose metabolism, immunity, and inflammation).
“Taken together, GW9662 influences genes in all classic PPARrelated metabolic pathways (lipid metabolism, glucose metabolism, immunity, and inflammation) (Clark, 2002;Wang, 2010).”
From The Peroxisome Proliferator–Activated Receptor (PPAR)-γ Antagonist 2-Chloro-5-Nitro-N-Phenylbenzamide (GW9662) Triggers Perilipin 2 Expression via PPARδ and Induces Lipogenesis and Triglyceride Accumulation in Human THP-1 Macrophages (2020) · cites this paper as Wang, 2010
The Introduction (page unavailable) describes PPARs as regulators of lipid metabolism and inflammation and discusses their relationship to insulin resistance. Our copy does not identify GW9662 or report that it influences genes in all the listed pathways, so it supports the PPAR-related background but not the claim about GW9662. (LLM, conf=0.78)
Experimental — accuracy not yet measuredPPARγ is predominantly expressed in adipose tissue and plays a central role in adipogenesis.
“PPARg is predominantly expressed in adipose tissue and plays a central role in adipogenesis (Wang, 2010).”
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References 117 · Cited by 366
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- Authors
- Wang, Y.-X.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Wang, Yong-Xu
- ORCID
- Wang, Yong-Xu
- Venue
- Cell Research
- Published
- 2010-01-26
- Volume
- 20
- Issue
- 2
- Pages
- 124-137
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- PMC
- PMC4084607
- OpenAlex
- W2126218858
- Cited by
- 366
- References
- 117
- Citations by year
- 2026: 25 · 2025: 23 · 2024: 31 · 2023: 24 · 2022: 35 · 2021: 30 · 2020: 32 · 2019: 24 · 2018: 23 · 2017: 14 · 2016: 20 · 2015: 18 · 2014: 13 · 2013: 17 · 2012: 23
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- American Diabetes Association
- Richard and Susan Smith Family Foundation
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK076118, R01DK076118)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- peroxisome proliferator-activated receptors, energy metabolism, energy homeostasis, metabolic disorders, metabolic syndrome, transcriptional regulation, PPAR ligands, nuclear receptors
- MeSH terms
- Animals, Energy Metabolism, Humans, Insulin Resistance, Metabolic Diseases, Models, Biological, Thiazolidinediones, Peroxisome Proliferator-Activated Receptors, Adipogenesis
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