为了探讨刺梨果酒对链脲佐菌素(STZ)诱导的1-型糖尿病大鼠糖代谢紊乱的影响及其作用机制。采用一次性腹腔注射STZ的方法建立1-型糖尿病大鼠模型，将造模成功后的大鼠分为刺梨果酒高、中、低剂量组和模型组，并设空白对照组。灌胃给药期间测定大鼠的饮食饮水量和体重，每2周测一次空腹血糖（FBG），实验期28 d。实验结束后测量血清胰岛素（Insulin，Ins）和果糖胺的含量；实时灾光定量PCR（real time polymerase chain reaction，RT-PCR）测定肝脏磷脂酞肌醇3-激酶(Phosphoinositide 3-kinase，PI3K)、蛋白激酶B（protein kinase B，Akt/PKB）和葡萄糖转运载体2（Glucose Transporter 2，GLUT2），以及骨骼肌葡萄糖转运载体4（Glucose Transporter 4，GLUT4）mRNA相对表达量。结果表明，与模型组相比，刺梨果酒高、中、低剂量组多饮多食的症状明显好转，体重下降受到抑制；刺梨果酒高、中、低剂量可显著（p<0.05）降低空腹血糖，分别下降了21.20%，36.14%和8.75%；果糖胺降低了11.32%，16.65%和8.33%；血清胰岛素水平分别上升了39.69%，45.87%和17.82%。与模型组相比，刺梨果酒高、中、低剂量组均可显著升高肝脏PI3K、PKB和GLUT2及骨骼肌GLUT4 mRNA相对表达量。本试验说明一定量的刺梨果酒具有改善STZ诱导的1-型糖尿病大鼠糖代谢紊乱，其中中剂量效果更明显。

To investigate the effect of Rosa roxburghii Tratt wine on the glucose metabolism disorder induced by streptozotocin (STZ) in type 1-diabetic rats, the type 1 diabetic rats model induced by intraperitoneal injection of STZ was established. The rats were randomly divided into blank group, model group, positive group, high, middle and low dose groups, blood glucose is measured every 2 weeks. After 28 days of administration, growth status and relative tissue weight were investigated. The contents of insulin (Ins) in serum were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of PI3K, PKB and GLUT2 in liver, and GLUT4 in skeletal muscle were determined by real time polymerase chain reaction (RT-PCR). The results showed that Rosa roxburghii Tratt wine significantly increase body weight and feed efficiency (p<0.05), significantly reduce fasting blood glucose (21.20%, 36.14% and 8.75%) and glucose tolerance (11.32%, 16.65% and 8.33%), relative tissue weight (p<0.05). when compared with model group. Moreover, Rosa roxburghii Tratt wine significantly increased mRNA relative expressions of PI3K, PKB and GLUT2 in liver and GLUT4 in skeletal muscle. In conclusion, Rosa roxburghii Tratt wine increased the concentration of Ins in serum of diabetic rats and reduced blood glucose levels. Its possible mechanism was that Rosa roxburghii Tratt wine promoted glucose uptake and utilization by activation of the Ins mediated PI3K pathway and translocation of GLUT2/4.

毕节市科技项目（毕科联合字ZY[2017]01号）；贵州省科技计划（黔科合平台人才[2018]5781-50）；贵州大学引进人才科研项目[贵大人基合字（2018）42号]