The DOI matches its Crossref record; 174 of the 174 references it cites were found in a registry or an index.
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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“the insulinsensitizing effects of thiazolidinediones, a class of PPARg ligands, are used for the treatment of type 2 diabetes mellitus (Tontonoz and Spiegelman, 2008;Hong et al., 2018).”
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
In the citing paper
“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
In the citing paper
“PPARs are activated by a variety of molecules and act mainly as sensors for fatty acids and fatty acid-derived metabolites (Lefebvre et al., 2006;Tontonoz and Spiegelman, 2008;Neels and Grimaldi, 2014).”
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
Citations
Cites
Obesity is associated with macrophage accumulation in adipose tissue
Weisberg, S. P., McCann, D., Desai, M., Rosenbaum, M., Leibel, R. L., & Ferrante, A. W. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319246 · Cited by 10,041
Adipose Expression of Tumor Necrosis Factor-α: Direct Role in Obesity-Linked Insulin Resistance
Hotamisligil, G. S., Shargill, N. S., & Spiegelman, B. M. (1993) · Science · doi:10.1126/science.7678183 · Cited by 7,518
Self-citationXu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., Sole, J., Nichols, A., Ross, J. S., Tartaglia, L. A., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319451 · Cited by 6,760
Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K., Mori, Y., Ide, T., Murakami, K., Tsuboyama-Kasaoka, N., et al. (2001) · Nature Medicine · doi:10.1038/90984 · Cited by 4,915
The hormone resistin links obesity to diabetes
Steppan, C. M., Bailey, S. T., Bhat, S., Brown, E. J., Banerjee, R. R., Wright, C. M., Patel, H. R., Ahima, R. S., & Lazar, M. A. (2001) · Nature · doi:10.1038/35053000 · Cited by 4,755
Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes
Nissen, S. E., & Wolski, K. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa072761 · Cited by 4,675
Yamauchi, T., Kamon, J., Minokoshi, Y., Ito, Y., Waki, H., Uchida, S., Yamashita, S., Noda, M., Kita, S., Ueki, K., et al. (2002) · Nature Medicine · doi:10.1038/nm788 · Cited by 4,238
Inflammation, stress, and diabetes
Wellen, K. E., & Hotamisligil, G. S. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25102 · Cited by 4,143
A Cold-Inducible Coactivator of Nuclear Receptors Linked to Adaptive Thermogenesis
Puigserver, P., Wu, Z., Park, C. W., Graves, R., Wright, M., & Spiegelman, B. M. (1998) · Cell · doi:10.1016/s0092-8674(00)81410-5 · Cited by 3,864
Self-citationLehmann, J. M., Moore, L. B., Smith-Oliver, T. A., Wilkison, W. O., Willson, T. M., & Kliewer, S. A. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.22.12953 · Cited by 3,645
Research works printed but not linked: 7
- Kletzien R, 1992, Mol. Pharmacol., 42, 558
- Harris P, 1994, Mol. Pharmacol., 45, 439
- 10.1210/me.11.6.779 · DOI
- 10.1172/JCI200525102 · DOI · Paper page
- 10.1016/j.expneurol.2006.04.006 · DOI
- 10.1210/en.142.7.3125 · DOI
- Suh N, 1999, Cancer Res., 59, 5671
Cited by
Sorted by citations
Mechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
Pathophysiology of human visceral obesity: an update
Tchernof, A., & Després, J.-P. (2013) · Physiological Reviews · doi:10.1152/physrev.00033.2011 · Cited by 2,583
EDC-2: the endocrine society's second scientific statement on endocrine-disrupting chemicals
Gore, A. C., Chappell, V. A., Fenton, S. E., Flaws, J. A., Nadal, A., Prins, G. S., Toppari, J., & Zoeller, R. T. (2015) · Endocrine Reviews · doi:10.1210/er.2015-1010 · Cited by 2,407
What we talk about when we talk about fat
Rosen, E. D., & Spiegelman, B. M. (2014) · Cell · doi:10.1016/j.cell.2013.12.012 · Cited by 2,373
Self-citationPPARγ signaling and metabolism: the good, the bad and the future
Ahmadian, M., Suh, J. M., Hah, N., Liddle, C., Atkins, A. R., Downes, M., & Evans, R. M. (2013) · Nature Medicine · doi:10.1038/nm.3159 · Cited by 2,016
Metadata
- 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 (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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 ›
Are you an author, or do you see a problem with this page? Request a review
