PPAR-α, a Lipid-Sensing Transcription Factor, Regulates Blood-Brain Barrier Efflux Transporter Expression
Open accessAbstract
Lipid sensor peroxisome proliferator-activated receptor alpha (PPAR- α) is the master regulator of lipid metabolism. Dietary release of endogenous free fatty acids, fibrates, and certain persistent environmental pollutants, e.g. perfluoroalkyl fire-fighting foam components, are peroxisome proliferator-activated receptor alpha ligands. Here, we define a role for peroxisome proliferator-activated receptor alpha in regulating the expression of three ATP-driven drug efflux transporters at the rat and mouse blood-brain barriers: P-glycoprotein (Abcb1), breast cancer resistance protein (Bcrp/Abcg2), and multidrug resistance-associated protein 2 (Mrp2/Abcc2). Exposing isolated rat brain capillaries to linoleic acid, clofibrate, or PKAs increased the transport activity and protein expression of the three ABC transporters. These effects were blocked by the PPAR- α antagonist, GW6471. Dosing rats with 20 mg/kg or 200 mg/kg of clofibrate decreased the brain accumulation of the P-glycoprotein substrate, verapamil, by 50% (in situ brain perfusion; effects blocked by GW6471) and increased P-glycoprotein expression and activity in capillaries ex vivo. Fasting C57Bl/6 wild-type mice for 24 h increased both serum lipids and brain capillary P-glycoprotein transport activity. Fasting did not alter P-glycoprotein activity in PPAR- α knockout mice. These results indicate that hyperlipidemia, lipid-lowering fibrates and exposure to certain fire-fighting foam components activate blood-brain barrier peroxisome proliferator-activated receptor alpha, increase drug efflux transporter expression and reduce drug delivery to the brain.
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A 2017 study using rats and mice found that PPARα agonists, including PFOS and PFNA, increased the expression and activity of these efflux transporters.
“A study from 2017 using rats and mice found that PPARα agonists, including PFOS and PFNA, increased the expression and activity of these efflux transporters.”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as More et al., 2017
The Results (page unavailable) show that PFOS and PFNA increased efflux-transporter activity in isolated rat brain capillaries, with effects varying by PFOS concentration. They do not report transporter-expression measurements for PFOS or PFNA, or tests of those compounds in mice; the mouse experiments used fasting. The cited paper is identified as a 2016 study, not a 2017 study. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPFAS exposure may have important implications for the treatment of certain ailments, such as brain cancer, epilepsy, and depression, through restriction of drug delivery.
“PFAS exposure may have important implications for the treatment of certain ailments, such as brain cancer, epilepsy, and depression (More et al., 2017; Kirk et al., 2021), through restriction of drug delivery.”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as More et al., 2017
The Results report that PFOS and PFNA increased drug-efflux transport in isolated rat brain capillaries, and the Discussion suggests this could restrict CNS drug delivery in humans. The paper does not specifically address treatment of brain cancer, epilepsy, or depression, so the disease-specific implications are not established by this source. (LLM, conf=0.85)
Experimental — accuracy not yet measuredPPARα is expressed at the BBB where it controls the expression of ATP-driven drug efflux transporters, such as P-glycoprotein, breast cancer resistance protein, and multidrug resistance-associated protein.
“PPARα is expressed at the BBB where it controls the expression of ATP-driven drug efflux transporters, such as P-glycoprotein (Abcb1), breast cancer resistance protein (Bcrp/Abcg2), and multidrug resistance-associated protein (Mrp2/Abcc2) (More et al., 2017).”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as More et al., 2017
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- Authors
- More, V. R., Campos, C. R., Evans, R. A., Oliver, K. D., Chan, G. N., Miller, D. S., & Cannon, R. E.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Cannon, Ronald E
- ORCID
- More, Vijay R
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2016-07-21
- Volume
- 37
- Issue
- 4
- Pages
- 1199-1212
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- PMC
- PMC5453444
- OpenAlex
- W2398366925
- Cited by
- 59
- References
- 49
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 8 · 2023: 10 · 2022: 5 · 2021: 11 · 2020: 7 · 2019: 6 · 2018: 3 · 2016: 2
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- PPARα, blood-brain barrier, efflux pumps, P-glycoprotein, ABCG2, MRP2, ABC transporters, clofibrate, linoleic acid, perfluorinated compounds, hyperlipidemia, fasting, verapamil, brain capillaries, GW6471, lipid metabolism, brain drug delivery
- MeSH terms
- ATP Binding Cassette Transporter, Subfamily G, Member 2, Multidrug Resistance-Associated Protein 2, Animals, Biological Transport, Blood-Brain Barrier, Brain, Capillaries, Clofibrate, Fasting, Fluorocarbons, Gene Expression Regulation, Male, Mice, Inbred C57BL, Oxazoles, Tyrosine, Rats, Sprague-Dawley, Alkanesulfonic Acids, Mice, Knockout, ATP-Binding Cassette Transporters, Linoleic Acid, ATP Binding Cassette Transporter, Subfamily B, Member 1, ATP-Binding Cassette, Sub-Family C Proteins, PPAR alpha
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