ArticleInternational journal of molecular sciences2021
P2Y2R Deficiency Ameliorates Hepatic Steatosis by Reducing Lipogenesis and Enhancing Fatty Acid β-Oxidation through AMPK and PGC-1α Induction in High-Fat Diet-Fed Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Liver Fibrosis and Purinergic Signaling: Autocrine-Paracrine Role of ATP in Liver Damage.International journal of molecular sciences · 2026Review
- Dicaffeoylquinic acid alleviates alcoholic liver disease by targeting PLA2G4B and inhibiting the MAPK signaling pathway.Frontiers in pharmacology · 2026Article
- Nuclear receptors in metabolic, inflammatory, and oncologic diseases: mechanisms, therapeutic advances, and future directions.European journal of medical research · 2025Review
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- Purinergic signaling in liver disease: calcium signaling and induction of inflammation.Purinergic signalling · 2025Review
- The role of natural products in improving lipid metabolism disorder-induced mitochondrial dysfunction of diabetic kidney disease.Frontiers in physiology · 2025Review
- Purinergic Signaling in Non-Parenchymal Liver Cells.International journal of molecular sciences · 2024Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Perilipin 5 regulates hepatic stellate cell activation and high-fat diet-induced non-alcoholic fatty liver disease.Animal models and experimental medicine · 2024Article
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- Erhong Jiangzhi Decoction Inhibits Lipid Accumulation and Alleviates Nonalcoholic Fatty Liver Disease with Nrf2 Restoration Under Obesity.Journal of inflammation research · 2024Article
- Article
- SIRT1 Activator E1231 Alleviates Nonalcoholic Fatty Liver Disease by Regulating Lipid Metabolism.Current issues in molecular biology · 2023Article
- Therapeutic potential for P2YPurinergic signalling · 2023Review
- Reduction of obesity and hepatic adiposity in high-fat diet-induced rats by besunyen slimming tea.Heliyon · 2023Article
- Knockout of Purinergic P2YInternational journal of molecular sciences · 2023Article
- Role of purinergic signalling in obesity-associated end-organ damage: focus on the effects of natural plant extracts.Frontiers in endocrinology · 2023Review
- Fatty acid metabolism: A new therapeutic target for cervical cancer.Frontiers in oncology · 2023Review
- Identification and validation of disulfidptosis-associated molecular clusters in non-alcoholic fatty liver disease.Frontiers in genetics · 2023Article
- Review
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8 authors at 1 institution in 1 country.
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Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic liver disease associated with obesity and insulin resistance. Activation of the purinergic receptor P2Y2R has been reported to promote adipogenesis, inflammation and dyslipidemia in adipose tissues in obese mice. However, the role of P2Y2R and its mechanisms in NAFLD remain unknown. We hypothesized that P2Y2R deficiency may play a protective role in NAFLD by modulating lipid metabolism in the liver. In this study, we fed wild type and P2Y2R knockout mice with a high-fat diet (HFD) for 12 weeks and analyzed metabolic phenotypes. First, P2Y2R deficiency effectively improved insulin resistance with a reduction in body weight and plasma insulin. Second, P2Y2R deficiency attenuated hepatic lipid accumulation and injury with reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Third, P2Y2R deficiency decreased the expression of fatty acid synthesis mediators (cluster of differentiation (CD36), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD1)); and increased the expression of adipose triglyceride lipase (ATGL), a lipolytic enzyme. Mechanistically, P2Y2R deficiency increased the AMP-activated protein kinase (AMPK) activity to improve mitochondrial fatty acid β-oxidation (FAO) by regulating acetyl-CoA carboxylase (ACC) and carnitine palmitoyltransferase 1A (CPT1A)-mediated FAO pathway. In addition, P2Y2R deficiency increased peroxisome proliferator-activated gamma co-activator-1α (PGC-1α)-mediated mitochondrial biogenesis. Conclusively, P2Y2R deficiency ameliorated HFD-induced hepatic steatosis by enhancing FAO through AMPK signaling and PGC-1α pathway, suggesting P2Y2R as a promising therapeutic target for NAFLD.
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