LGALS12, also known as galectin12, belongs to the galectin family with β-galactoside-binding activity. We previously reported that LGALS12 is an important regulator of adipogenesis in porcine adipocytes in vitro, but its value in pig breeding needed to be explored in vivo. In this study, we used CRISPR/Cas9 to construct porcine fetal fibroblasts (PFFs) with a 43 bp deletion in LGALS12 exon 2. Using these PFFs as donor cells, a LGALS12 knockout pig model was generated via somatic cell nuclear transfer. Primary cultures of porcine intramuscular (IM) and subcutaneous (SC) adipocytes were established using cells from LGALS12 knockout pigs and wild-type pigs. A comparison of these cells proved that LGALS12 deficiency suppresses cell proliferation via the RAS-p38MAPK pathway and promotes lipolysis via the PKA pathway in both IM and SC adipocytes. In addition, we observed AKT activation only in IM adipocytes and suppression of the Wnt/β-catenin only in SC adipocytes. Our findings suggest that LGALS12 deficiency affects the adipogenesis of IM and SC adipocytes through different mechanisms.

LGALS12，也称为半乳糖凝集素12，属于半乳糖凝集素家族，具有β-半乳糖苷结合活性。我们之前报道LGALS12在体外是猪脂肪细胞脂肪生成的重要调节因子，但其在猪育种中的价值需要在体内探索。在本研究中，我们使用CRISPR/Cas9构建了LGALS12外显子2中43 bp缺失的猪胎儿成纤维细胞（PFF）。使用这些PFF作为供体细胞，通过体细胞核移植生成了LGALS12基因敲除猪模型。使用来自 LGALS12 敲除猪和野生型猪的细胞建立猪肌内 (IM) 和皮下 (SC) 脂肪细胞的原代培养物。对这些细胞的比较证明，LGALS12 缺陷可通过 RAS-p38MAPK 途径抑制细胞增殖，并通过 PKA 途径促进 IM 和 SC 脂肪细胞的脂肪分解。此外，我们仅在 IM 脂肪细胞中观察到 AKT 激活，仅在 SC 脂肪细胞中观察到 Wnt/β-catenin 抑制。我们的研究结果表明，LGALS12 缺陷通过不同的机制影响 IM 和 SC 脂肪细胞的脂肪生成。