Adiponectin receptor agonist AdipoRon suppresses adipogenesis in C3H10T1/2 cells through the adenosine monophosphate-activated protein kinase signaling pathway

The aim of the present study was to investigate the effects of AdipoRon, an adiponectin receptor agonist, on adipogenesis in C3H10T1/2 cells and to explore the underlying mechanisms. C3H10T1/2 cells were treated with increasing doses of AdipoRon for 8 days, and Oil Red O staining was used to assess lipid accumulation. The protein and mRNA expression levels of adipogenic transcription factors and adipocyte-specific genes were examined by western blotting and reverse transcription quantitative polymerase chain reaction, respectively. AdipoRon treatment inhibited lipid accumulation in C3H10T1/2 cells in a dose-dependent manner and significantly suppressed the expression of adipogenic transcription factors, including peroxisome proliferator-activated recepto gamma, CAAT/enhancer binding protein (C/EBP)-beta and C/EBP alpha. In addition, cells treated with AdipoRon exhibited a significant decrease in the expression of adipocyte-specific genes, including fatty acid binding protein 4, fatty acid synthase, leptin, adiponectin, and stearoyl-CoA desaturase-1. Notably, AdipoRon significantly increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). The results indicated that AdipoRon exerted an inhibitory effect on adipogenesis in C3H10T1/2 cells by downregulating the expression of adipogenic transcription factors and adipocyte-specific genes and by promoting the phosphorylation of AMPK and ACC, which suggested that AdipoRon may be a potential drug to prevent and treat diseases caused by abnormal adipogenesis, such as obesity.