Trial reportPsychopharmacology2020
PPARγ activation by pioglitazone does not suppress cravings for alcohol, and is associated with a risk of myopathy in treatment seeking alcohol dependent patients: a randomized controlled proof of principle study.
Trial report in Psychopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01631630 (Role of Proinflammatory Signaling in Alcohol Craving), which is not on this map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Role of Proinflammatory Signaling in Alcohol Craving
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Pioglitazone for the treatment of alcohol use disorder: A randomized controlled trial.Addiction (Abingdon, England) · 2026Trial
- Inflammatory endotoxin challenge in individuals with alcohol use disorder and controls.Alcohol, clinical & experimental research · 2025Trial
- Pharmacologic management of metabolic and alcohol-associated liver disease.Metabolism and target organ damage · 2026Article
- Novel medications for problematic alcohol use.The Journal of clinical investigation · 2024Review
- Promising immunomodulators for management of substance and alcohol use disorders.Expert opinion on pharmacotherapy · 2024Review
- A reverse translational study of PPAR-α agonist efficacy in human and rodent models relevant to alcohol use disorder.Neurobiology of stress · 2024Article
- Neuroimmune modulators as novel pharmacotherapies for substance use disorders.Brain, behavior, & immunity - health · 2024Article
- 24-Norursodeoxycholic acid ameliorates experimental alcohol-related liver disease and activates hepatic PPARγ.JHEP reports : innovation in hepatology · 2023Article
- Low Dopamine D2 Receptor Expression Drives Gene Networks Related to GABA, cAMP, Growth and Neuroinflammation in Striatal Indirect Pathway Neurons.Biological psychiatry global open science · 2023Article
- The vicious cycle between (neuro)inflammation and alcohol use disorder: An opportunity to develop new medications?Alcohol, clinical & experimental research · 2023Article
- Endotoxin for Alcohol Research: A Call for Experimental Medicine Using Lipopolysaccharide Challenge.Alcohol and alcoholism (Oxford, Oxfordshire) · 2021Article
- Repurposing Peroxisome Proliferator-Activated Receptor Agonists in Neurological and Psychiatric Disorders.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Immune treatments for alcohol use disorder: A translational framework.Brain, behavior, and immunity · 2021Review
- Improving translation of animal models of addiction and relapse by reverse translation.Nature reviews. Neuroscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleProinflammatory processes have been implicated in alcohol addiction, craving, and relapse, while studies in experimental animals have suggested that activation of peroxisome proliferator-activated receptor gamma (PPARγ) inhibits proinflammatory signaling. Accordingly, it is hypothesized that medications with PPARγ activity may have therapeutic potential in alcohol dependence.
objectivesWe conducted a double-blind, placebo-controlled mechanistic proof of principle study in alcohol-dependent inpatients to investigate the effect of pioglitazone on alcohol craving.
methodsParticipants were treated for withdrawal, if needed, and then randomized to pioglitazone (target dose 45 mg/day) or placebo. Once at target dose, they completed two experimental manipulations: guided imagery, which used personalized auditory scripts to induce alcohol cravings, and a low-dose challenge with i.v. lipopolysaccharide (LPS; 0.8 ng/kg) or placebo, on two separate sessions, in counterbalanced order. Behavioral and endocrine responses as well as CSF levels of proinflammatory cytokines were evaluated.
resultsThe study was prematurely terminated after randomization of 16 subjects, following an independent review that established a high risk of myopathy in the active treatment group. Analysis of those who completed the study indicated that pioglitazone was associated with elevated, rather than suppressed alcohol cravings in response to alcohol-associated stimuli. LPS did not induce cravings for alcohol and thus did not lend itself to evaluating pioglitazone effects; however, pioglitazone increased the neuroendocrine stress response to LPS. CSF levels of IL-6, TNF-α, or MCP-1 were unaffected by pioglitazone treatment.
conclusionsBoth safety and efficacy biomarker data suggest that pioglitazone lacks potential as a medication for the treatment of alcohol dependence. CLINICAL
trial registrationNCT01631630.
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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.