Adiponectin receptor agonist reduces broiler hepatic lipid deposition

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.