Abstract

Long non-coding RNAs (lncRNAs) are important regulators of adipogenesis and energy metabolism, but their roles in visceral fat deposition remain incompletely understood. Here, we investigated the function of the rabbit lncRNA RRP12-AS and evaluated the conservation of its human homolog using in vitro and in vivo gain- and loss-of-function models. RRP12-AS promoted rabbit adipocyte proliferation but inhibited adipogenic differentiation, while in vivo overexpression reduced perirenal fat hypertrophy and improved lipid metabolic parameters. Mechanistically, RRP12-AS interacted with hnRNPA1 and enhanced UCP1 expression by regulating UCP1 mRNA stability and translation efficiency, thereby promoting thermogenesis in adipose tissue. In addition, the human homolog H-RRP12-AS showed similar regulatory effects on cellular lipid metabolism. Together, these findings identify RRP12-AS as a regulator of visceral fat metabolism through the hnRNPA1/UCP1 axis and suggest its potential relevance as a therapeutic target for central obesity.