RESUMEN
Salusinß and adiponectin receptor 1 (adipoR1) serve important roles in the development of certain cardiovascular diseases and lipid metabolism. However, to the best of our knowledge, the relationship between salusinß and adipoR1, and their underlying mechanisms of action, currently remain unclear. In the present study, lentiviral vectors designed to overexpress salusinß or knock down salusinß expression were used in 293T and HepG2 cells. Semiquantitative PCR was performed to investigate the relationship between salusinß and adipoR1 mRNA expression in 293T cells. Western blotting was used to assess the protein expression levels of adipoR1, adenosine monophosphateactivated protein kinase (AMPK), acetylCoA carboxylase (ACC) and carnitine palmitoyl transferase 1A (CPT1A) in transfected HepG2 cells. Simultaneously, HepG2 cells were treated with an adipoR1 inhibitor (thapsigargin) or agonist (AdipoRon) and the resultant changes in the expression levels of the aforementioned proteins were observed. Oil Red O staining and measurements of cellular triglyceride levels were performed to assess the extent of lipid accumulation in HepG2 cells. The results demonstrated that salusinß overexpression downregulated adipoR1 expression and inhibited the phosphorylation of AMPK and ACC, which led to decreased CPT1A protein expression. By contrast, salusinß knockdown increased adipoR1 expression and promoted the phosphorylation of AMPK and ACC, which conversely enhanced CPT1A protein expression. Treatment with adipoR1 agonist, AdipoRon, reversed the effects of salusinß overexpression. In addition, salusinß overexpression enhanced intracellular lipid accumulation in HepG2 cells induced by free fatty acid treatment. These findings highlighted the potential regulatory role of salusinß in adipoR1mediated signaling pathways. To conclude, the present study provided insights into the regulation of fatty acid metabolism by the liver. In particular, salusinß may serve as a potential target for the therapeutic intervention of metabolic disorders of lipids.