Uridine has formerly been shown to alleviate obesity and hepatic lipid accumulation. N-carbamoyl aspartate (NCA) provides carbon atoms to uridine in de novo pyrimidine biosynthesis pathway. However, whether NCA is involved in the lipid metabolism remains elusive. Here we showed that NCA supplementation significantly decreased (P < 0.05) serum cholesterol (CHOL), high-density lipoprotein (HDL), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) levels of mice, and significantly increased (P < 0.05) relative mRNA expression of genes related to the synthesis of pyrimidine nucleotides and polyunsaturated fatty acids. Besides, supplemented with NCA significantly decreased body weight and area under the curve (AUC), and increased body temperature in the high-fat diet fed mice. For further, relative protein expression of uridine monophosphate synthase (UMPS), sterol regulatory element-binding protein 1(SREBP-1) and phosphorylated hormone-sensitive triglyceride lipase (P-HSL) in the liver, and uncoupling protein 1 (UCP-1) in interscapular brown adipose tissue (iBAT) also showed upregulated in the high-fat diet fed mice. Thus, NCA promoted de novo synthesis of pyrimidine and polyunsaturated fatty acid, and reduced body weight by stimulating high-fat diet-induced thermogenesis of iBAT.

尿苷以前被证明可以减轻肥胖和肝脏脂质积累。N-氨基甲酰天冬氨酸 (NCA) 在从头嘧啶生物合成途径中为尿苷提供碳原子。然而，NCA 是否参与脂质代谢仍不清楚。在这里，我们发现补充 NCA 可显着降低 ( P  < 0.05)小鼠血清胆固醇(CHOL)、高密度脂蛋白 (HDL)、乳酸脱氢酶 (LDH) 和碱性磷酸酶 (ALP) 水平，并显着升高 ( P  < 0.05) ) 嘧啶核苷酸合成相关基因的相对mRNA表达和多不饱和脂肪酸。此外，补充 NCA 可显着降低高脂肪饮食喂养小鼠的体重和曲线下面积 (AUC)，并提高体温。进一步，肝脏中尿苷单磷酸合酶（UMPS）、甾醇调节元件结合蛋白1（SREBP-1）和磷酸化激素敏感性甘油三酯脂肪酶（P-HSL）以及解偶联蛋白1（UCP-1）的相对蛋白表达) 在肩胛间棕色脂肪组织 (iBAT) 中也显示在高脂肪饮食喂养的小鼠中上调。因此，NCA 促进了嘧啶和多不饱和脂肪酸的从头合成，并通过刺激高脂肪饮食诱导的 iBAT 产热来减轻体重。