College of Biological and Chemical Engineering, Jiaxing University, Jiaxing, China.
College of Agronomy and Biotechnology, Hebei Normal University of Science and Technology, Qinhuangdao, China.
Acta Biochim Biophys Sin (Shanghai). 2018 Oct 1;50(10):960-967. doi: 10.1093/abbs/gmy099.
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.
增加肌肉内（IM）脂肪，同时减少皮下（SC）脂肪含量是猪种选育的主要目标之一。鉴定参与脂质代谢的基因对实现这一目标至关重要。半乳糖凝集素 12（LGALS12）已被证明是调节小鼠模型脂肪沉积的重要因子；然而，LGALS12 对猪脂肪生成的影响和调控机制尚不清楚。在这项研究中，通过猪 SC 和 IM 脂肪原代培养细胞探索了 LGALS12 对脂肪沉积的影响。对不同组织中 LGALS12 表达的分析表明，LGALS12 主要在脂肪组织中表达。还评估了 LGALS12 在脂肪细胞分化阶段的表达模式，发现 SC 和 IM 脂肪之间存在差异。设计了 LGALS12 的小干扰 RNA（siRNA）并转染到源自 SC 和 IM 脂肪的猪脂肪细胞中。转染后，LGALS12 的表达水平显著降低，SC 和 IM 脂肪来源的脂肪细胞中的脂滴数量减少。同时，脂肪生成标志物，包括 PPARγ 和 aP2 的水平降低，而水解标志物，包括脂肪甘油三酯脂肪酶（ATGL）和激素敏感脂肪酶（HSL）的水平升高。此外，在 SC 和 IM 来源的终末分化脂肪细胞中，观察到 LGALS12 敲低后脂解信号的激活，如 PKA 和 Erk1/2 的磷酸化。综上所述，这些结果表明，LGALS12 敲低可以通过下调脂肪生成基因和激活 PKA-Erk1/2 信号通路来抑制猪脂肪细胞的脂肪生成。
