Long noncoding RNAs (lncRNAs) are emerging as critical regulators of metabolic homeostasis and obesity pathogenesis. Mitochondrial dysfunction is a key driver of metabolic disorders, yet the underlying regulatory mechanisms remain incompletely understood. In this study, we unveil the metabolic function of a novel lncRNA GM44386 (LncRNA11), which is abundantly expressed in brown adipose tissue and functions as a protective molecule against obesity-related energy imbalance. Genetic deletion of LncRNA11 in mice led to exacerbated adipocyte hypertrophy, insulin resistance, and severe hepatic lipid accumulation under both normal and high-fat diet (HFD) conditions. Functionally, LncRNA11 deficiency compromised mitochondrial structure, quality, and oxidative phosphorylation capacity in adipocytes, resulting in defective fatty acid oxidation and impaired thermogenesis. Mechanistically, LncRNA11 forms a complex with Heterogeneous Nuclear Ribonucleoprotein A1 (hnRNPA1) to potentiate mitochondrial glycolysis in adipose tissue by upregulating pyruvate kinase M (PKM) expression. This enhancement supplies ATP required for UCP1-mediated uncoupling, thereby helping to maintain mitochondrial integrity and adaptive thermogenesis. Collectively, our findings identify LncRNA11 as a crucial upstream regulator that coordinates thermogenic capacity and mitochondrial stability, presenting a potential therapeutic target for combating obesity.