{"title":"Adiponectin receptor agonist reduces broiler hepatic lipid deposition.","authors":"Wenhao Tan, Kunyu Jiang, Yuhan Zhang, Hang Gao, Xingyi Tang, Sha Jiang","doi":"10.3389/fvets.2025.1667501","DOIUrl":null,"url":null,"abstract":"<p><p>To investigate the effects of AdipoRon on fatty liver syndrome (FLS) in chicken, we used a corticosterone (CORT)-induced fatty liver model in Cobb broilers <i>in vivo</i> and fat emulsion-induced model in Leghorn male hepatoma cells (LMH) <i>in vitro</i>. In the <i>in vivo</i> study, eighteen 33-day-old male Cobb broilers were randomly assigned to three groups: control group (CONT, vehicle), corticosterone-treated group (CORT, 4 mg/kg), and corticosterone with AdipoRon-treated group (CORT-AR, 4 mg/kg and 0.2 mg/kg, 1 time/1 day) for 5 days. The results showed AdipoRon reduced CORT-induced increase in liver crude fat content (<i>p</i> < 0.05), increased protein expressions of peroxisome proliferator-activated receptor <i>α</i> (PPARα) (<i>p</i> < 0.05) and adiponectin (ADPN) (<i>p</i> < 0.05), and suppressed the protein expressions of Acetyl-CoA carboxylase 1 (ACC) (<i>p</i> < 0.05) and phosphorylated c-Jun N-terminal kinase 1 (p-JNK1) (<i>p</i> < 0.05) in the liver. In the <i>in vitro</i> study, LMH cells were divided into control (CN), fat emulsion (FE, 10%), and FE + AdipoRon (4 μM) group (FE-AR). AdipoRon reduced FE-induced lipid accumulation (<i>p</i> < 0.05), decreased the protein expression of ACC and tumor necrosis factor-alpha (TNF-<i>α</i>), and enhanced PPARα, the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK), and carnitine palmitoyl transferase 1 (CPT-1) (<i>p</i> < 0.05). In conclusion, AdipoRon effectively reduces hepatic lipid deposition in CORT-induced FLS broilers, likely through PPARα activation and inhibition of lipid synthesis via ACC downregulation.</p>","PeriodicalId":12772,"journal":{"name":"Frontiers in Veterinary Science","volume":"12 ","pages":"1667501"},"PeriodicalIF":2.9000,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491982/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Veterinary Science","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.3389/fvets.2025.1667501","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
To investigate the effects of AdipoRon on fatty liver syndrome (FLS) in chicken, we used a corticosterone (CORT)-induced fatty liver model in Cobb broilers in vivo and fat emulsion-induced model in Leghorn male hepatoma cells (LMH) in vitro. In the in vivo study, eighteen 33-day-old male Cobb broilers were randomly assigned to three groups: control group (CONT, vehicle), corticosterone-treated group (CORT, 4 mg/kg), and corticosterone with AdipoRon-treated group (CORT-AR, 4 mg/kg and 0.2 mg/kg, 1 time/1 day) for 5 days. The results showed AdipoRon reduced CORT-induced increase in liver crude fat content (p < 0.05), increased protein expressions of peroxisome proliferator-activated receptor α (PPARα) (p < 0.05) and adiponectin (ADPN) (p < 0.05), and suppressed the protein expressions of Acetyl-CoA carboxylase 1 (ACC) (p < 0.05) and phosphorylated c-Jun N-terminal kinase 1 (p-JNK1) (p < 0.05) in the liver. In the in vitro study, LMH cells were divided into control (CN), fat emulsion (FE, 10%), and FE + AdipoRon (4 μM) group (FE-AR). AdipoRon reduced FE-induced lipid accumulation (p < 0.05), decreased the protein expression of ACC and tumor necrosis factor-alpha (TNF-α), and enhanced PPARα, the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK), and carnitine palmitoyl transferase 1 (CPT-1) (p < 0.05). In conclusion, AdipoRon effectively reduces hepatic lipid deposition in CORT-induced FLS broilers, likely through PPARα activation and inhibition of lipid synthesis via ACC downregulation.
期刊介绍:
Frontiers in Veterinary Science is a global, peer-reviewed, Open Access journal that bridges animal and human health, brings a comparative approach to medical and surgical challenges, and advances innovative biotechnology and therapy.
Veterinary research today is interdisciplinary, collaborative, and socially relevant, transforming how we understand and investigate animal health and disease. Fundamental research in emerging infectious diseases, predictive genomics, stem cell therapy, and translational modelling is grounded within the integrative social context of public and environmental health, wildlife conservation, novel biomarkers, societal well-being, and cutting-edge clinical practice and specialization. Frontiers in Veterinary Science brings a 21st-century approach—networked, collaborative, and Open Access—to communicate this progress and innovation to both the specialist and to the wider audience of readers in the field.
Frontiers in Veterinary Science publishes articles on outstanding discoveries across a wide spectrum of translational, foundational, and clinical research. The journal''s mission is to bring all relevant veterinary sciences together on a single platform with the goal of improving animal and human health.