目的:本研究试图研究β-rophin与某些关键酶的关系,即乳酸脱氢酶-5(LDH5),柠檬酸合成酶(CS),和乙酰辅酶A羧化酶-1(ACC1),在胰岛素抵抗小鼠中。
方法:本研究使用8周龄雄性C57BL6/J小鼠(实验组n=10,对照组n=10)。使用渗透泵施用S961以在小鼠中诱导胰岛素抵抗。betatrophin,LDH5,CS,使用实时聚合酶链反应(RT-PCR)方法从小鼠的肝脏中确定ACC1表达水平。此外,生化参数,如血清betatrophin,空腹血糖,胰岛素,甘油三酯,总胆固醇,分析高密度脂蛋白(HDL)和低密度脂蛋白(LDL)胆固醇水平。
结果:betatrophin表达与血清betatrophin(p=0.000),空腹血糖,胰岛素,甘油三酯(p≤0.001),实验组总胆固醇(p=0.013)水平升高。此外,实验组CS基因表达水平显著下降(p=0.01)。尽管发现其表达与血清betatrophin和甘油三酯水平之间有很强的相关性,betatrophin基因表达与LDH5,ACC1和CS基因表达水平无相关性.
结论:betatrophin水平似乎在调节甘油三酯代谢中起重要作用,而胰岛素抵抗会增加betatrophin基因表达和血清水平,并降低CS表达水平。研究结果表明,betatrophin可能不通过CS和LDH5调节碳水化合物代谢或直接通过ACC1酶调节脂质代谢。
OBJECTIVE: The present study sought to examine the relationship of betatrophin with certain key enzymes, namely lactate dehydrogenase-5 (LDH5), citrate synthase (CS), and acetyl-CoA carboxylase-1 (ACC1), in insulin-resistant mice.
METHODS: Eight-week-old male C57BL6/J mice were used in this study (experimental group n=10 and control group n=10). S961 was administered using an osmotic pump to induce insulin resistance in the mice. The betatrophin, LDH5, CS, and ACC1 expression levels were determined from the livers of the mice using the real-time polymerase chain reaction (RT-PCR) method. Moreover, biochemical parameters such as the serum betatrophin, fasting glucose, insulin, triglyceride, total cholesterol, and high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol levels were analyzed.
RESULTS: The betatrophin expression and serum betatrophin (p=0.000), fasting glucose, insulin, triglyceride (p≤0.001), and total cholesterol (p=0.013) levels were increased in the experimental group. In addition, the CS gene expression level was statistically significantly decreased in the experimental group (p=0.01). Although strong correlation was found between the expression and serum betatrophin and triglyceride levels, no correlation was found between the betatrophin gene expression and the LDH5, ACC1, and CS gene expression levels.
CONCLUSIONS: The betatrophin level appears to play an important role in the regulation of triglyceride metabolism, while insulin resistance increases both the betatrophin gene expression and serum levels and decreases the CS expression level. The findings suggest that betatrophin may not regulate carbohydrate metabolism through CS and LDH5 or lipid metabolism directly through the ACC1 enzyme.