ArticleAlcoholism, clinical and experimental research2016
PPAR Agonists: I. Role of Receptor Subunits in Alcohol Consumption in Male and Female Mice.
Article in Alcoholism, clinical and experimental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Fenofibrate restores glutamatergic and dopaminergic homeostasis in the nucleus accumbens and reduces alcohol relapse in rats.Frontiers in pharmacology · 2026Article
- Novel medications for problematic alcohol use.The Journal of clinical investigation · 2024Review
- Inhibition of the Sodium-Calcium Exchanger Reverse Mode Activity Reduces Alcohol Consumption in Rats.International journal of molecular sciences · 2024Article
- Fenofibrate Decreases Ethanol-Induced Neuroinflammation and Oxidative Stress and Reduces Alcohol Relapse in Rats by a PPAR-α-Dependent Mechanism.Antioxidants (Basel, Switzerland) · 2023Article
- Effect of a brain-penetrant selective estrogen receptor degrader (SERD) on binge drinking in female mice.Alcoholism, clinical and experimental research · 2022Article
- Immune treatments for alcohol use disorder: A translational framework.Brain, behavior, and immunity · 2021Review
- Review
- Effects of Pharmacologically Targeting Neuroimmune Pathways on Alcohol Drinking in Mice Selectively Bred to Drink to Intoxication.Alcoholism, clinical and experimental research · 2020Article
- Endocannabinoid-Like Lipid Neuromodulators in the Regulation of Dopamine Signaling: Relevance for Drug Addiction.Frontiers in synaptic neuroscience · 2020Review
- A Pathway-Based Genomic Approach to Identify Medications: Application to Alcohol Use Disorder.Brain sciences · 2019Article
- Neuroimmune signaling in alcohol use disorder.Pharmacology, biochemistry, and behavior · 2019Review
- Several behavioral traits relevant for alcoholism are controlled by ɣ2 subunit containing GABANeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- From gene networks to drugs: systems pharmacology approaches for AUD.Psychopharmacology · 2018Review
- Medications for alcohol use disorders: An overview.Pharmacology & therapeutics · 2018Review
- In vivo interactions between α7 nicotinic acetylcholine receptor and nuclear peroxisome proliferator-activated receptor-α: Implication for nicotine dependence.Neuropharmacology · 2017Article
- The peroxisome proliferator-activated receptor alpha agonist fenofibrate attenuates alcohol self-administration in rats.Neuropharmacology · 2017Article
- Inflammatory responses to alcohol in the CNS: nuclear receptors as potential therapeutics for alcohol-induced neuropathologies.Journal of leukocyte biology · 2016Review
- Preclinical Medication Development: New Targets and New Drugs.Alcoholism, clinical and experimental research · 2016Review
- PPAR Agonists: II. Fenofibrate and Tesaglitazar Alter Behaviors Related to Voluntary Alcohol Consumption.Alcoholism, clinical and experimental research · 2016Article
- Genes and Alcohol Consumption: Studies with Mutant Mice.International review of neurobiology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSeveral peroxisome proliferator-activated receptor (PPAR) agonists reduce voluntary alcohol consumption in rodent models, and evidence suggests that PPARα and γ subunits play an important role in this effect. To define the subunit dependence of this action, we tested selective PPARα and α/γ agonists and antagonists in addition to null mutant mice lacking PPARα.
methodsThe effects of fenofibrate (PPARα agonist) and tesaglitazar (PPARα/γ agonist) on continuous and intermittent 2-bottle choice drinking tests were examined in male and female wild-type mice and in male mice lacking PPARα. We compared the ability of MK886 (PPARα antagonist) and GW9662 (PPARγ antagonist) to inhibit the effects of fenofibrate and tesaglitazar in wild-type mice. The estrogen receptor antagonist, tamoxifen, can inhibit PPARγ-dependent transcription and was also studied in male and female mice.
resultsFenofibrate and tesaglitazar reduced ethanol (EtOH) consumption and preference in wild-type mice, but these effects were not observed in mice lacking PPARα. MK886 inhibited the action of fenofibrate, but not tesaglitazer, while GW9662 did not inhibit either agonist. The PPAR agonists were more effective in male mice compared to females, and drinking in the continuous 2-bottle choice test was more sensitive to fenofibrate and tesaglitazar compared to drinking in the intermittent access test. Tamoxifen also reduced EtOH consumption in male mice and this action was inhibited by GW9662, but not MK886, suggesting that it acts by activation of PPARγ.
conclusionsOur study using selective PPAR agonists, antagonists, and null mutant mice indicates a key role for PPARα in mediating reduced EtOH consumption by fenofibrate and tesaglitazar.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.