Knockdown of LGALS12 inhibits porcine adipocyte adipogenesis via PKA-Erk1/2 signaling pathway.

Increasing intramuscular (IM) fat while concomitantly decreasing subcutaneous (SC) fat content is one major goal of pig breeding. Identifying genes involved in lipid metabolism is critical for this goal. Galectin-12 (LGALS12) has been proven to be an important regulator of fat deposition in mouse models; however, the effect and regulatory mechanisms of LGALS12 on porcine adipogenesis are still unknown. In this study, the effects of LGALS12 on fat deposition were explored with primary culture of porcine SC and IM adipocytes. Analysis of LGALS12 expression across different tissues revealed that LGALS12 was predominantly expressed in adipose tissue. The LGALS12 expression patterns across stages of adipocyte differentiation were also evaluated, with differences observed between SC and IM fat. Small interfering RNA (siRNA) of LGALS12 was designed and transfected into porcine adipocytes derived from SC and IM fat. After transfection, the expression level of LGALS12 was significantly reduced, and the number of lipid droplets was reduced in adipocytes from both SC and IM fat. Simultaneously, the levels of adipogenic markers, including PPARγ and aP2, were decreased, whereas hydrolysis markers, including adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were increased. Furthermore, the activation of lipolysis signals, such as the phosphorylation of PKA and Erk1/2, were observed with LGALS12 knockdown in terminally differentiated adipocytes from both SC and IM sources. Taken together, these results suggest that LGALS12 knockdown can inhibit adipogenesis of porcine adipocytes by downregulating lipogenic genes and activating the PKA-Erk1/2 signaling pathway.