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PPARs, Obesity, and Inflammation
Open accessAbstract
The worldwide prevalence of obesity and related metabolic disorders is rising rapidly, increasing the burden on our healthcare system. Obesity is often accompanied by excess fat storage in tissues other than adipose tissue, including liver and skeletal muscle, which may lead to local insulin resistance and may stimulate inflammation, as in steatohepatitis. In addition, obesity changes the morphology and composition of adipose tissue, leading to changes in protein production and secretion. Some of these secreted proteins, including several proinflammatory mediators, may be produced by macrophages resident in the adipose tissue. The changes in inflammatory status of adipose tissue and liver with obesity feed a growing recognition that obesity represents a state of chronic low-level inflammation. Various molecular mechanisms have been implicated in obesity-induced inflammation, some of which are modulated by the peroxisome proliferator-activated receptors (PPARs). PPARs are ligand-activated transcription factors involved in the regulation of numerous biological processes, including lipid and glucose metabolism, and overall energy homeostasis. Importantly, PPARs also modulate the inflammatory response, which makes them an interesting therapeutic target to mitigate obesity-induced inflammation and its consequences. This review will address the role of PPARs in obesity-induced inflammation specifically in adipose tissue, liver, and the vascular wall.
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“The anti-inflammatory activities of PPARs are partially effectuated by inhibition of NF-κB. PPARs are able to attenuate NF-κB function either by interfering with the transcription activating capacity of the NF-κB complex or by regulating genes that suppress the activation of NF-κB. By physical interaction with components of the NF-κB complex, PPARα impairs binding of NF-κB to the DNA and”
From Antioxidant and Anti-Inflammatory Activities of Essential Oils: A Short Review (2010) · cites this paper as [134]
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Metadata
- Authors
- Stienstra, R., Duval, C., Müller, M., & Kersten, S.
- Affiliations
- Wageningen University & Research (NL)
- Corresponding author
- Kersten, Sander
- Venue
- PPAR Research
- Publisher
- Hindawi Limited
- Published
- 2007
- Volume
- 2007
- Pages
- 1-10
- ISSN
- 1687-4757 (ISSN-L)
- 1687-4765
- PMC
- PMC1783744
- OpenAlex
- W1963979793
- Cited by
- 287
- References
- 98
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 14 · 2023: 24 · 2022: 14 · 2021: 23 · 2020: 23 · 2019: 12 · 2018: 13 · 2017: 12 · 2016: 16 · 2015: 10 · 2014: 14 · 2013: 22 · 2012: 23
- FWCI
- 5.30
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PPAR Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Socio-Environmental Systems Modeling (acceptedVersion)
- UEA Digital Repository (University of East Anglia) (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Radboud Repository (Radboud University) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- peroxisome proliferator-activated receptors, obesity, inflammation, adipose tissue, liver, steatohepatitis, insulin resistance, macrophages, pro-inflammatory mediators, vascular inflammation, energy homeostasis, metabolic disorders, therapeutic target
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