Genetic Variation Determines PPARγ Function and Anti-diabetic Drug Response In Vivo
Open accessAbstract
SNPs affecting disease risk often reside in non-coding genomic regions. Here, we show that SNPs are highly enriched at mouse strain-selective adipose tissue binding sites for PPARγ, a nuclear receptor for anti-diabetic drugs. Many such SNPs alter binding motifs for PPARγ or cooperating factors and functionally regulate nearby genes whose expression is strain selective and imbalanced in heterozygous F1 mice. Moreover, genetically determined binding of PPARγ accounts for mouse strain-specific transcriptional effects of TZD drugs, providing proof of concept for personalized medicine related to nuclear receptor genomic occupancy. In human fat, motif-altering SNPs cause differential PPARγ binding, provide a molecular mechanism for some expression quantitative trait loci, and are risk factors for dysmetabolic traits in genome-wide association studies. One PPARγ motif-altering SNP is associated with HDL levels and other metabolic syndrome parameters. Thus, natural genetic variation in PPARγ genomic occupancy determines individual disease risk and drug response.
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Assisted loading has been described in various systems.
“Assisted loading has been described in various systems30–37.”
From Synergistic gene expression during the acute phase response is characterized by transcription factor assisted loading (2017) · cites this paper as [34]
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- Authors
- Soccio, R. E., Chen, E. R., Rajapurkar, S. R., Safabakhsh, P., Marinis, J. M., Dispirito, J. R., Emmett, M. J., Briggs, E. R., Fang, B., Everett, L. J., Lim, H.-W., Won, K.-J., Steger, D. J., Wu, Y., Civelek, M., Voight, B. F., & Lazar, M. A.
- Affiliations
- University of Pennsylvania (US)
- University of North Carolina at Chapel Hill (US)
- University of California, Los Angeles (US)
- Corresponding author
- Lazar, Mitchell A.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 162
- Issue
- 1
- Pages
- 33-44
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4493773
- OpenAlex
- W1511590367
- Cited by
- 117
- References
- 53
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 2 · 2023: 3 · 2022: 9 · 2021: 10 · 2020: 11 · 2019: 13 · 2018: 14 · 2017: 16 · 2016: 20 · 2015: 7
- FWCI
- 8.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institutes of Health (5r01dk049780-29)
- National Heart, Lung, and Blood Institute (R00HL121172, K99HL121172, P01HL028481)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 49780, R01DK098542, R01-DK049780, F30DK104513, R01DK101478, R21DK098769, P01DK049210, K08DK094968, P30 DK 19525, P30DK019525, T32DK007314)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- PPARγ, single nucleotide polymorphisms, nuclear receptor binding sites, adipose tissue, thiazolidinediones, drug response, mouse strain differences, expression quantitative trait loci, HDL cholesterol, metabolic syndrome, personalized medicine
- MeSH terms
- Adipose Tissue, Animals, Humans, Hypoglycemic Agents, Mice, Inbred C57BL, Transcription Factors, Gene Expression, Polymorphism, Single Nucleotide, PPAR gamma, Mice, Mice, 129 Strain
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