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目的探讨脑室内高水平Nesfatin-1(1-82)重组蛋白对大鼠糖脂代谢及其相关酶的影响。方法构建大鼠第三脑室微量输注系统将大鼠分为Nesfatin-1蛋白输注组(A组)和人工脑脊液输注组(B组),采用扩展胰岛素钳夹术评定Nesfatin-1蛋白对肝糖脂代谢的影响,采用RT-PCR和酶动力学方法测定葡萄糖-6-磷酸酶(G-6-P)和磷酸烯醇式丙酮酸羧激酶(PEPCK mRNA)表达和活性变化。结果在钳夹稳定状态下,A组葡萄糖输注率(GIR)高于B组[(28.3±1.4)vs(23.0±1.8)mg/(kg.min),P<0.01]。A组葡萄糖清除率(GRd)高于B组[(34.9±1.3)vs(31.8±1.8)mg/(kg.min),P<0.01]。RT-PCR结果显示,A组PEPCK mRNA表达与PEPCK酶活性均低于B组。结论中枢Nesfatin-1(1-82)短期灌注增加了大鼠机体IS,并抑制了肝糖异生。
Objective To investigate the effects of intracerebral high level Nesfatin-1 (1-82) recombinant protein on glucose and lipid metabolism and related enzymes in rats. Methods The third ventricle microinfusion system was established. The rats were divided into Nesfatin-1 protein infusion group (A group) and artificial cerebrospinal fluid infusion group (B group), and the extended insulin clamp was used to evaluate the Nesfatin-1 protein The effects of glucose-6-phosphatase (G-6-P) and phosphoenolpyruvate carboxykinase (PEPCK mRNA) on hepatic glucose and lipid metabolism were determined by RT-PCR and enzyme kinetic methods. Results In the steady state of clamp, the GIR of group A was higher than that of group B [(28.3 ± 1.4) vs (23.0 ± 1.8) mg / (kg · min), P <0.01]. The glucose clearance (GRd) in group A was significantly higher than that in group B [(34.9 ± 1.3) vs (31.8 ± 1.8) mg / (kg · min), P <0.01]. RT-PCR results showed that the expression of PEPCK mRNA and the activity of PEPCK in group A were lower than those in group B. Conclusion Short-term central Nesfatin-1 (1-82) infusion increases IS and inhibits hepatic gluconeogenesis in rats.