ArticleCurrent research in food science2020
Piceatannol attenuates fat accumulation and oxidative stress in steatosis-induced HepG2 cells.
Article in Current research in food science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Lipid metabolic reprogramming of tumor-associated macrophages drives resistance to immune checkpoint blockade in lung cancer: a narrative review of mechanisms and therapeutic strategies.Translational lung cancer research · 2026Review
- MicroRNA-34a Promotes Hepatic Lipid Accumulation Through RXRα Suppression and Is Reversed by 9-International journal of molecular sciences · 2026Article
- Passiflora edulis f. flavicarpa Extract Prevents Muscle Atrophy and Insulin Resistance in High-Fat Diet-Induced Obese Rats via Regulating the Nrf2, NF-κB, and IRS-1/PI3K/AKT Signaling Pathways.Oxidative medicine and cellular longevity · 2026Article
- Taurine attenuates lipid accumulation via the eCB-CB1 axis: evidence from adipose metabolomics in HFD-fed mice and 3D adipocyte spheroids.Frontiers in nutrition · 2026Article
- Natural Compounds TargetingNutrients · 2025Review
- Seven days of piceatannol supplementation exerted no effect on fat metabolism at rest, during and after exercise.Journal of clinical biochemistry and nutrition · 2025Article
- Quinoa Polyphenol Extract Alleviates Non-Alcoholic Fatty Liver Disease via Inhibiting Lipid Accumulation, Inflammation and Oxidative Stress.Nutrients · 2024Article
- Regulation and targeting of SREBP-1 in hepatocellular carcinoma.Cancer metastasis reviews · 2024Review
- Natural compounds targeting nuclear receptors for effective cancer therapy.Cancer metastasis reviews · 2023Review
- The Antiproliferative Activity ofMolecules (Basel, Switzerland) · 2023Article
- Therapeutic Potential of Phenolic Compounds in Medicinal Plants-Natural Health Products for Human Health.Molecules (Basel, Switzerland) · 2023Review
- Diagnostic and therapeutic strategies for non-alcoholic fatty liver disease.Frontiers in pharmacology · 2022Review
- Biological Mechanisms and Related Natural Inhibitors of CD36 in Nonalcoholic Fatty Liver.Drug design, development and therapy · 2022Review
- Constituent Characteristics and Functional Properties of Passion Fruit Seed Extract.Life (Basel, Switzerland) · 2021Review
- Role of stilbenes against insulin resistance: A review.Food science & nutrition · 2021Review
- CCL4-mediated targeting of spleen tyrosine kinase (Syk) inhibitor using nanoparticles alleviates inflammatory bowel disease.Clinical and translational medicine · 2021Article
- Therapeutic Targeting of Nonalcoholic Fatty Liver Disease by Downregulating SREBP-1C ExpressionFrontiers in molecular biosciences · 2021Article
- The Gut Barrier, Intestinal Microbiota, and Liver Disease: Molecular Mechanisms and Strategies to Manage.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD), which affects over 20% of the adult population, is the most common liver disease worldwide and can progress to inflammatory hepatitis, cirrhosis and liver cancer. The need to alleviate NAFLD is imperative, but there are limited pharmacological therapies available. Based on previous reports that piceatannol, a stilbenoid metabolite of resveratrol, exhibits anti-obesity, antioxidant and anti-inflammatory effects, the goal of this study was to determine the efficacy of piceatannol on prevention and/or treatment of NAFLD. The results showed that piceatannol significantly decreased fat accumulation and suppressed lipogenesis and fatty acids (FAs) uptake by decreasing sterol regulatory element-binding protein 1 (SREBP1) and cluster of differentiation 36 (CD36) in steatosis-induced HepG2 hepatocytes. Piceatannol treatment also promoted FAs β-oxidation by increasing farnesoid X receptor (FXR), peroxisome proliferator-activated receptor α (PPARα), and carnitine palmitoyltransferase 1α (CPT1α) under steatosis conditions. Moreover, piceatannol significantly suppressed FA-induced oxidative stress and inhibited phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinases 1/2 (ERK1/2). Overall, it is suggested that piceatannol reduced fat accumulation in steatosis-induced HepG2 cells by suppressing lipogenesis (SREBP1 and ACC) and FA uptake (CD36), and promoting FAs oxidation (FXR, PPARα and CPT1α).
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