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

Abstract

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 8days, 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 receptorγ, CAAT/enhancer binding protein (C/EBP)‑β and C/EBPα. 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.