Adiponectin receptor agonist reduces broiler hepatic lipid deposition.

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 broilersand fat emulsion-induced model in Leghorn male hepatoma cells (LMH). In thestudy, eighteen 33-day-old male Cobb broilers were randomly assigned to three groups: control group (CONT, vehicle), corticosterone-treated group (CORT, 4&#x202f;mg/kg), and corticosterone with AdipoRon-treated group (CORT-AR, 4&#x202f;mg/kg and 0.2&#x202f;mg/kg, 1 time/1&#x202f;day) for 5&#x202f;days. The results showed AdipoRon reduced CORT-induced increase in liver crude fat content (&#x202f;<&#x202f;0.05), increased protein expressions of peroxisome proliferator-activated receptor(PPAR&#x3b1;) (&#x202f;<&#x202f;0.05) and adiponectin (ADPN) (&#x202f;<&#x202f;0.05), and suppressed the protein expressions of Acetyl-CoA carboxylase 1 (ACC) (&#x202f;<&#x202f;0.05) and phosphorylated c-Jun N-terminal kinase 1 (p-JNK1) (&#x202f;<&#x202f;0.05) in the liver. In thestudy, LMH cells were divided into control (CN), fat emulsion (FE, 10%), and FE&#x202f;+&#x202f;AdipoRon (4&#x202f;&#x3bc;M) group (FE-AR). AdipoRon reduced FE-induced lipid accumulation (&#x202f;<&#x202f;0.05), decreased the protein expression of ACC and tumor necrosis factor-alpha (TNF-), and enhanced PPAR&#x3b1;, the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK), and carnitine palmitoyl transferase 1 (CPT-1) (&#x202f;<&#x202f;0.05). In conclusion, AdipoRon effectively reduces hepatic lipid deposition in CORT-induced FLS broilers, likely through PPAR&#x3b1; activation and inhibition of lipid synthesis via ACC downregulation.