Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease worldwide, imposing a substantial disease burden. Long non-coding ribonucleic acid (lncRNA) have been demonstrated to be extensively involved in the regulation of lipid metabolism. However, current studies have mainly focused on liver-derived lncRNA, while the mechanism by which adipose tissue-derived lncRNA affects hepatic lipid metabolism through exosome-mediated inter-organ pathways remains unclear. LINC01705 is a newly identified functional lncRNA produced by adipocytes. Under metabolic stress conditions such as high glucose, LINC01705 is packaged into exosomes and delivered to hepatocytes, where it sponges microRNA (miR)-552-3p through a competing endogenous RNA mechanism, thereby relieving the transcriptional repression of liver X receptor α, activating downstream lipogenic pathways, and promoting lipid accumulation in hepatocytes. This article focuses on LINC01705 and systematically reviews its biological characteristics and regulatory mechanisms in the development and progression of MASLD, with particular emphasis on its inter-organ regulatory features of being “adipocyte-derived, exosome-mediated and liver-targeted”. The relationship between adipose tissue and the liver and its clinical significance are further explored at the molecular level, with the aim of providing a reference for research in this field.