Abstract
Many Long non-coding RNAs (lncRNAs) are specifically expressed in early embryos, but the physiological functions of most of them remain largely unknown. Here, we show that deficiency of lncenc1, an early embryo-specific lncRNA, altering glucose and lipid balance in adult mice. Newly weaned lncenc1-deficient mice prefer to use lipids as a fuel source. When mice were fed a normal chow diet (NCD), glucose intolerance and insulin resistance were observed in adult lncenc1-deficient mice. Under high-fat diet (HFD) conditions, however, lncenc1-deficient mice became healthier and could resist food-induced obesity and metabolic disturbances. Furthermore, AKT/mTOR-regulated lipogenesis in liver was reduced in lncenc1-deficient mice fed a HFD. MEFs lacking lncenc1 showed impaired glycolysis and lipogenesis, suggesting that the metabolic defects may already exist in embryos. Our study demonstrated the essential roles of lncenc1 in adult metabolism, providing experimental data that support the "fetal origin" of adult metabolic disorders.