The liver coordinately maintains cholesterol, triglyceride, and glucose homeostasis by integrating the synthesis, storage, utilization, and inter-conversion of these metabolic programs, and their dysregulation contributes to metabolic-associated steatotic liver disease (MASLD), hepatocellular carcinoma (HCC), type 2 diabetes mellitus (T2DM), and gestational diabetes mellitus (GDM). Long non-coding RNAs (lncRNAs), which are not translated into proteins, regulate gene expression through interactions with DNA, RNA, and proteins at transcriptional, post-transcriptional, and epigenetic levels, and have emerged as central determinants of hepatic metabolic balance. This review systematically summarizes how lncRNAs govern cholesterol biosynthesis and efflux, triglyceride synthesis and lipolysis, glycogen turnover, gluconeogenesis, and glycolysis in hepatocytes. Unlike pathway-by-pathway descriptions, we highlight that these programs are coupled through shared signaling networks, including PI3K/AKT/mechanistic target of rapamycin complex 1 (mTORC1), 5′-AMP-activated protein kinase (AMPK), SREBP, PPAR, and FoxO1, and that pleiotropic lncRNAs coordinate lipid and glucose outputs rather than controlling a single isolated process. We further examine how lncRNA dysregulation drives MASLD, HCC, T2DM, and GDM, and evaluate their potential as diagnostic biomarkers and therapeutic targets. Finally, we outline current limitations, including incomplete molecular characterization, low cross-species conservation, heterogeneous experimental validation, and unresolved delivery challenges, which must be addressed before lncRNA-based strategies reach clinical application.