Tail adipose deposition in sheep is an economically significant trait that has an impact on meat quality and reproductive performance. This study elucidates the regulatory mechanism of FGFBP1 in the proliferation and differentiation of ovine tail-derived preadipocytes. Overexpression and knockdown methods were used to establish gain- and loss-of-function models, and the biological effects of FGFBP1 on adipocyte dynamics were systematically assessed. FGFBP1 overexpression significantly inhibited cellular proliferation by cell cycle arrest in the G2/M phase, and, at the same time, promoted adipocyte differentiation by upregulating key adipogenic markers (PPARγ, Adiponectin, C/EBPα, and FABP4). In contrast, gene silencing enhanced the proliferative capacity and decreased lipid droplet accumulation, confirming its inhibitory role in adipogenesis. Our findings indicate that FGFBP1 is a key regulator of tail adipogenesis. This discovery enhances our understanding of the mechanisms of adipocyte differentiation and provides theoretical bases and potential therapeutic targets for optimizing lipid deposition traits in livestock production.

Skeletal muscle, accounting for about 40% of the body’s mass, is an important trait for farm animal production. Skeletal muscle satellite cells (MuSCs) are an excellent material for studying the regulatory mechanisms underlying muscle growth and regeneration after birth. Here, we analyzed the role and underlying mechanisms of Myc-associated zinc finger protein (MAZ) and secretory leukocyte protease inhibitor (SLPI) in porcine MuSC (pMuSC) proliferation for the first time. It was revealed that both MAZ and SLPI advanced the proliferation of pMuSCs by promoting cell cycle progression, and that a MAZ/SLPI axis regulated pMuSC proliferation. It was further shown that this MAZ/SLPI axis regulated pMuSC proliferation through the Wnt/β-catenin pathway. The proliferative role obtained above was confirmed in mouse myoblast C2C12 cells. Additionally, a single-nucleotide polymorphism (SNP), −360C>T, which frequently occurred in the promoter of the SLPI gene from Min, Yorkshire, and Longmin black pigs, was found to significantly increase the gene’s expression in vitro and in vivo. The SNP −360C>T in SLPI is a potential molecular marker predicting the proliferative ability of pMuSCs. The data provide a basis for controlling muscle growth and regeneration, which will provide benefits for improving the meat production of pigs and controlling muscle-related diseases in humans.