Nesfatin-1对1型糖尿病小鼠糖脂代谢和外周神经病变作用

THE EFFECT OF NESFATIN-1 ON GLYCOLIPID METABOLISM AND PERIPHERAL NEUROPATHY IN MOUSE WITH TYPE 1 DIABETES MELLITUS

目的探究外周Nesfatin-1能否通过调节糖脂代谢从而改善1型糖尿病(T1DM)小鼠的神经病变。方法将小鼠随机分为生理盐水对照组(C+NS组)、Nesfatin-1对照组(C+Nesfatin-1组)、生理盐水模型组(DM+NS组)和Nesfatin-1模型组(DM+Nesfatin-1组),连续6d小鼠尾静脉给予20μg/kg Nesfatin-1或等体积生理盐水。比较各组T1DM小鼠摄食、体质量变化,血糖、血脂水平,胰岛和肝脏形态结构,腓肠肌AMPK mRNA和GLUT4mRNA表达及甩尾潜伏期变化。结果 Nesfatin-1可显著降低T1DM小鼠血糖(F=24.79,q=5.91,P<0.01),但不影响给药后24h累计摄食量和体质量;能够保护胰岛结构完整性,促进肝脏脂质分解;可促进腓肠肌AMPK mRNA表达(F=8.57,q=6.25,P<0.05);能够缩短T1DM小鼠甩尾潜伏期(F=19.92,q=4.82,P<0.01)。结论外周Nesfatin-1可通过调节T1DM小鼠糖脂代谢从而改善外周神经病变。

Objective To probe if peripheral Nesfatin-1 can improve neuropathy in mouse with type 1 diabetes mellitus （T1DM） through regulating glycolipid metabolism. Methods The mice in this study were randomized to four groups as normal saline control group, Nesfatin-1 control group, normal saline model group and Nesfatin-i model group. The mice were treated with caudal vein transfusion of Nesfatin-1 （20 /μg/kg） or equal-volume normal saline accordingly for six days. A comparison was done among the mice that received Nesfatin-1 and those received no Nesfatin-1 with regard to ingestion, body weight, blood glucose, blood fat, morphosis of islet and liver, AMPK mRNA, GLUT4 mRNA of gastrocnemius and tail-flick latency. Results Nesfa- tin-1 significantly decreased blood sugar level in mice with T1DM （F= 24.79,q = 5.91, P〈0.01）, but did not affect the 24-hour to- tal food intake and body weight, could protect structural integrity of islet and promote lipid decomposition in liver, advance AMPK mRNA expression （F=8.57,q=6.25,P〈0.05）, and shorten tail-flick latency （F=19.92,q=4.82,P〈0.01）. Conclusion Pe- ripheral Nesfatin-lcan improves peripheral neuropathy in mice with T1DM by way of regulating their glycolipid metabolism.