SOCS2, a member of suppressor of cytokine signaling (SOCS) family, is a negative regulator of the signal pathway Janus kinase/signal transducers and activators of transcription (JAK/STAT). Growth hormone (GH) could stimulate lipolysis in adipose tissue. To demonstrate the specific influence of SOCS2 on porcine adipocytes differentiation and lipid metabolism induced by GH, we induced porcine primary adipocytes with 500 ng/ml GH and then tested the triglyceride (TG) accumulation and mRNA expressions of crucial genes in lipid metabolism like peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), SOCS2 and SOCS3. Then we retested these genes expressions in different time point after further treatment that over expressed SOCS2 in primary adipocytes and treated with 500 ng/ml GH. Results showed 500 ng/ml GH significantly restrained the porcine primary adipocytes differentiation. Specifically, 0.5 h after the induction with GH, accumulation of TG began to increase, and turned down since 8 h after. GH could promote PPARγ and FAS expressions during earlier stage (0-1 h), restrain from 4 h. However, ATGL and HSL mRNA expressions were stabile increasing. The expression of SOCS2 increased steadily after GH stimulation while SOCS3 expression was instantaneous rise. Overexpression of SOCS2 significantly decreased GH-induced the increase of PPARγ, FAS, ATGL and HSL mRNA expressions in earlier stage (0-1 h), as well as FAS and ATGL protein expression. Otherwise SOCS2 overexpression significantly decreased signal transducers and activators of transcription 3 (STAT3), signal transducers and activators of transcription 5 (STAT5) mRNA expressions and tyrosine phosphorylation levels with GH stimulation. At the same time SOCS3 mRNA kept in a lower level in Ad-SOCS2 transfected adipocytes. In conclusion, SOCS2 might be an important negative regulator of GH signaling in porcine adipocytes, which would provide the ground work for the mechanism of SOCS2 regulation fat metabolism.