Fat and Beyond: The Diverse Biology of PPARγ
Abstract
The nuclear receptor PPARgamma is a ligand-activated transcription factor that plays an important role in the control of gene expression linked to a variety of physiological processes. PPARgamma was initially characterized as the master regulator for the development of adipose cells. Ligands for PPARgamma include naturally occurring fatty acids and the thiazolidinedione (TZD) class of antidiabetic drugs. Activation of PPARgamma improves insulin sensitivity in rodents and humans through a combination of metabolic actions, including partitioning of lipid stores and the regulation of metabolic and inflammatory mediators termed adipokines. PPARgamma signaling has also been implicated in the control of cell proliferation, atherosclerosis, macrophage function, and immunity. Here, we review recent advances in our understanding of the diverse biological actions of PPARgamma with an eye toward the expanding therapeutic potential of PPARgamma agonist drugs.
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PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity.
“as PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity, while PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [113]
Both PPAR-γ and PPAR-δ activation may prove beneficial in maintaining metabolic flexibility during aging.
“Both PPAR-γ and PPAR-δ activation may prove beneficial in maintaining metabolic flexibility during aging”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [113]
PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis.
“as PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity, while PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [113]
PPARγ exerts considerable effects on lipid and glucose metabolism and insulin sensitivity.
“In addition, PPARg exerts considerable effects on lipid and glucose metabolism and insulin sensitivity (Tontonoz and Spiegelman, 2008).”
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 Tontonoz and Spiegelman, 2008
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Mechanisms underlying inflammation in neurodegeneration
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- Authors
- Tontonoz, P., & Spiegelman, B. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Harvard University (US)
- Venue
- Annual Review of Biochemistry
- Publisher
- Annual Reviews
- Published
- 2008-06-01
- Volume
- 77
- Issue
- 1
- Pages
- 289-312
- ISSN
- 0066-4154 (ISSN-L)
- 1545-4509
- OpenAlex
- W2097511872
- Cited by
- 2,085
- References
- 173
- Citations by year
- 2026: 79 · 2025: 100 · 2024: 104 · 2023: 103 · 2022: 111 · 2021: 106 · 2020: 105 · 2019: 108 · 2018: 110 · 2017: 112 · 2016: 135 · 2015: 125 · 2014: 154 · 2013: 160 · 2012: 149
- FWCI
- 8.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Heart, Lung, and Blood Institute (R01HL066088, HL66088)
- National Institute of Diabetes and Digestive and Kidney Diseases (R37 DK 3140)
- 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, transcriptional regulation, adipose tissue development, thiazolidinediones, insulin sensitivity, adipokines, lipid partitioning, atherosclerosis, macrophage function, immunity, cell proliferation, PPARγ agonists, antidiabetic drugs
- MeSH terms
- Animals, Cell Nucleus, Humans, Inflammation, Insulin Resistance, Macrophages, Models, Biological, Models, Molecular, Neoplasms, Protein Conformation, Protein Structure, Tertiary, Adipocytes, Thiazolidinediones, PPAR gamma, Adipogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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