Adiponectin promotes preadipocyte differentiation via the PPARγ pathway

According to the results of a preliminary study, it was hypothesized that the effects of adiponectin (APN) on the improvement of atherosclerosis may be associated with adipocyte differentiation and peroxisome proliferator‑activated receptor γ (PPARγ). The present study simulated the inflammatory environment of epicardial adipose tissue by stimulating mature adipocytes with lipopolysaccharide (LPS); subsequently, the differentiation of 3T3‑L1 preadipocytes was observed. 3T3‑L1 preadipocytes were infected with an adenovirus containing the human adiponectin gene apM1 (Ad‑apM1) and were co‑cultured with mature adipocytes stimulated with LPS. Differentiation into mature adipocytes was initiated using differentiation medium. After 8 days, an MTT assay was used to examine cell viability and oil red O staining was used to observe preadipocyte differentiation. In addition, the mRNA expression levels of monocyte chemoattractant protein‑1 (MCP‑1), interleukin (IL)‑6, IL‑8 and tumor necrosis factor α (TNF‑α) were examined by quantitative polymerase chain reaction, and the protein expression levels of PPARγ, CCAAT/enhancer binding protein α (C/EBPα) and preadipocyte factor‑1 (Pref‑1) were measured by western blotting. The results indicated that APN overexpression significantly increased preadipocyte differentiation and cell viability, inhibited MCP‑1, IL‑6, IL‑8 and TNF‑α expression, upregulated PPARγ and C/EBPα expression, and downregulated Pref‑1 under LPS stimulation. In addition, inhibition of PPARγ activity by T0070907 markedly attenuated the effects of APN overexpression. Taken together, the present study demonstrated that the effects of APN on the promotion of preadipocyte differentiation under inflammatory conditions may involve the PPARγ signaling pathway, and at least partly depends on upregulation of PPARγ expression.