ArticleScientific reports2021
Allopurinol ameliorates high fructose diet induced hepatic steatosis in diabetic rats through modulation of lipid metabolism, inflammation, and ER stress pathway.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Long-Term Fructose Intake Induces Moderate Liver Inflammation but Does not Overlap with the Detrimental Effects of the Ketogenic Diet on Hepatic Steatosis in Rats.Inflammation · 2026Article
- Allopurinol Use Is Associated with Decreased Incidence of Hepatic Decompensation and Overall Mortality among Individuals with Cirrhosis: A Propensity-Matched Cohort Study.GE Portuguese journal of gastroenterology · 2025Article
- Curcumin's dual effect on pyroptosis and autophagy in metabolic- associated fatty liver disease: a potential therapeutic strategy.Scientific reports · 2025Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease: A Silent Driver of Cardiovascular Risk and a New Target for Intervention.International journal of molecular sciences · 2025Review
- The effect of adipose-derived mesenchymal stem cells against high fructose diet induced liver dysfunction and dysbiosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Hyperuricemia-induced complications: dysfunctional macrophages serve as a potential bridge.Frontiers in immunology · 2025Review
- Article
- Metabolic dysfunction-associated steatotic liver disease and cardiovascular risk: a comprehensive review.Cardiovascular diabetology · 2024Review
- Review
- Review
- Serum uric acid and nonalcoholic fatty liver disease.Frontiers in endocrinology · 2024Review
- LINC01705 derived from adipocyte exosomes regulates hepatocyte lipid accumulation via an miR-552-3p/LXR axis.Journal of diabetes investigation · 2023Article
- Sestrin2: multifaceted functions, molecular basis, and its implications in liver diseases.Cell death & disease · 2023Review
- Convergence of Fructose-Induced NLRP3 Activation with Oxidative Stress and ER Stress Leading to Hepatic Steatosis.Inflammation · 2023Article
- Article
- Article
- Emerging Role of NLRP3 Inflammasome and Pyroptosis in Liver Transplantation.International journal of molecular sciences · 2022Review
- Dietary Ferulic Acid Ameliorates Metabolism Syndrome-Associated Hyperuricemia in RatsFrontiers in nutrition · 2022Article
- Allopurinol Use and the Risk of Type 2 Diabetes Mellitus: A Meta-Analysis of Cohort Studies.Dose-response : a publication of International Hormesis SocietyArticle
- THE THERAPEUTIC EFFECT OF ALLOPURINOL IN FATTY LIVER DISEASE IN RATS.Acta endocrinologica (Bucharest, Romania : 2005)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excess fructose consumption contributes to development obesity, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). Uric acid (UA), a metabolite of fructose metabolism, may have a direct role in development of NAFLD, with unclear mechanism. This study aimed to evaluate role of fructose and UA in NAFLD and explore mechanisms of allopurinol (Allo, a UA lowering medication) on NAFLD in Otsuka Long-Evans Tokushima Fatty (OLETF) rats fed a high fructose diet (HFrD), with Long-Evans Tokushima Otsuka (LETO) rats used as a control. There were six groups: LETO, LETO-Allo, OLETF, OLETF-Allo, OLETF-HFrD, and OLETF-HFrD-Allo. HFrD significantly increased body weight, epididymal fat weight, and serum concentrations of UA, cholesterol, triglyceride, HbA1c, hepatic enzymes, HOMA-IR, fasting insulin, and two hour-glucose after intraperitoneal glucose tolerance tests, as well as NAFLD activity score of liver, compared to the OLETF group. Allopurinol treatment significantly reduced hepatic steatosis, epididymal fat, serum UA, HOMA-IR, hepatic enzyme levels, and cholesterol in the OLETF-HFrD-Allo group. Additionally, allopurinol significantly downregulated expression of lipogenic genes, upregulated lipid oxidation genes, downregulated hepatic pro-inflammatory cytokine genes, and decreased ER-stress induced protein expression, in comparison with the OLETF-HFrD group. In conclusion, allopurinol ameliorates HFrD-induced hepatic steatosis through modulation of hepatic lipid metabolism, inflammation, and ER stress pathway. UA may have a direct role in development of fructose-induced hepatic steatosis, and allopurinol could be a candidate for prevention or treatment of NAFLD.
Indexed as
Identifiers
What OpenQuestion holds
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.