Transcriptome analysis of healthy and fatty liver revealed that inhibition of SLCO1B3 induces abnormal liver metabolism and lipid synthesis.

The liver serves as the central organ for lipid metabolism, making it a crucial component of chicken physiology. However, the intricate regulation of lipid absorption, synthesis, decomposition, and transport within the liver is influenced by various factors, such as environmental conditions, diet, and genetics. Recent research has suggested that numerous functional genes and transcription factors play a pivotal role in liver metabolism via different molecular mechanisms. In this study, we examined the transcriptomes of both healthy and fatty chicken livers to better understand the role of functional genes in chicken liver fat metabolism. Our bioinformatics analysis of RNA-seq data revealed differential expression of SLCO1B3 in healthy liver and fatty liver, with lower ex-pression levels observed in fatty liver. To further investigate the potential role of SLCO1B3 in liver metabolism, we conducted in vitro experiments to knock down its expression in primary hepatocytes. Our results indicated that SLCO1B3 could suppress lipogenesis, hepatocyte apoptosis, and inflammation. These findings provide insight into the molecular mechanism of SLCO1B3 as a functional gene capable of regulating fat metabolism in chicken liver, and may contribute to ad-dressing the issue of fatty liver in chicken.