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.

许多长非编码RNA（lncRNA）在早期胚胎中特异表达，但其中大多数的生理功能仍然未知。在这里，我们表现出的缺乏lncenc1在成年小鼠，早期胚胎特异性lncRNA的，改变血糖和血脂的平衡。刚断奶的lncenc1缺陷小鼠更喜欢使用脂质作为燃料来源。当给小鼠喂食正常的食物（NCD）时，在成年lncenc1缺陷小鼠中观察到了葡萄糖耐量和胰岛素抵抗。然而，在高脂饮食（HFD）条件下，缺乏lncenc1的小鼠变得更健康，可以抵抗食物引起的肥胖症和代谢紊乱。此外，Lncenc1减少了AKT / mTOR调节的肝脏脂肪生成缺陷的小鼠饲喂HFD。缺少lncenc1的MEFs表现出糖酵解和脂肪形成受损，表明代谢缺陷可能已经存在于胚胎中。我们的研究证明了lncenc1在成人新陈代谢中的重要作用，提供了支持成人新陈代谢疾病“胎儿起源”的实验数据。