MiR-432 mediates bidirectional regulation in the determination of adipocyte fate

Fat deposition represents a fundamental physiological process in mammalian energy metabolism, yet its molecular regulatory mechanisms remain incompletely understood. Adipocytes, the primary site of fat storage, develop through proliferation and differentiation of preadipocytes-a process controlled by multiple molecular regulators. MicroRNAs (miRNAs) act as crucial post-transcriptional regulators and play an essential role in mammalian adipogenesis. However, their specific functions in ovine tail fat deposition remain poorly characterized. This study aimed to systematically investigate the regulatory role of miR-432 in adipogenesis using sheep tail fat as a model system. Through establishing an in vitro preadipocyte culture model and implementing gain- and loss-of-function approaches via miRNA overexpression and antisense oligonucleotide inhibition, we demonstrated that elevated expression of miR-432 significantly enhanced preadipocyte proliferation, accompanied by upregulation of proliferation-related genes (Cyclin D, PCNA). However, it decreased lipid droplet accumulation and reduced the expression of differentiation markers (PPARγ, FABP4). Conversely, inhibition of miR-432 reduced cellular proliferation, downregulated key cell cycle genes (CCNB1, Cyclin B3), and enhanced adipogenic differentiation, as evidenced by increased lipid droplet formation and elevated expression of adipogenic genes (PPARγ, Adiponectin, FABP4). These findings demonstrate that miR-432 exerts a dual regulatory role in sheep tail adipogenesis by modulating both proliferative and differentiative processes in adipocytes. This research provides novel molecular insights into the regulatory mechanisms underlying fat deposition.