Testosterone Inhibits Lipid Accumulation in Porcine Preadipocytes by Regulating

Castration is commonly used to reduce stink during boar production. In porcine adipose tissue, castration reduces androgen levels resulting in metabolic disorders and excessive fat deposition. However, the underlying detailed mechanism remains unclear. In this study, we constructed porcine preadipocyte models with and without androgen by adding testosterone exogenously. The fluorescence intensity of lipid droplet (LD) staining and the fatty acid synthetase () mRNA levels were lower in the testosterone-treated cells than in the untreated control cells. In contrast, the mRNA levels of adipose triglycerides lipase () and androgen receptor () were higher than in the testosterone-treated cells than in the control cells. Subsequently, transcriptomic sequencing of porcine preadipocytes incubated with and without testosterone showed that the mRNA expression levels of very long-chain fatty acid elongase 3 (), a key enzyme involved in fatty acids synthesis and metabolism, were high in control cells. The siRNA-mediated knockdown of reduced LD accumulation and the mRNA levels of and increased the mRNA levels of . Next, we conducted dual-luciferase reporter assays using wild-type and mutant promoter reporters, which showed that the promoter contained an androgen response element (ARE); furthermore, its transcription was negatively regulated by overexpression. In conclusion, our study reveals that testosterone inhibits fat deposition in porcine preadipocytes by suppressing expression. Moreover, our study provides a theoretical basis for further studies on the mechanisms of fat deposition caused by castration.