胰腺衍生因子在糖尿病小鼠胰腺中的表达

摘要

目的 探讨胰腺衍生因子(PANDER)在1型和2型糖尿病小鼠胰岛中的表达变化及其与胰岛素抵抗和高血糖的相关性.方法 以STZ诱导和自发性Akita 1型糖尿病小鼠及2型糖尿病db/db小鼠为动物模型,用实时定量PCR,免疫组化和Western blot的方法检测胰腺中PANDER mRNA和蛋白指标.结果 相较于正常C57BL/6小鼠,STZ诱导和Akita 1型糖尿病小鼠胰腺组织中PANDER mRNA( STZ:1.00±0.17 vs0.25±0.06,P ＜0.01；Akita；1.00±0.19 vs 0.17±0.04,P＜0.001)和蛋白(免疫组化灰度扫描STZ:1.00±0.18 vs 0.16±0.11)水平均明显降低；相较于db/m小鼠,db/db小鼠胰腺组织中PANDER mRNA(1.00±0.05 vs 2.13±0.46,P＜0.05)和蛋白(1.00±0.28vs 3.58±0.36,P＜0.01)水平均明显升高；罗格列酮灌胃db/db小鼠1个月后,胰岛肥大、胰岛素抵抗及高血糖症状得以缓解,同时胰腺中PANDER mRNA( 1.00±0.13 vs 0.28±0.06,P＜0.01)和蛋白水平明显降低.结论 1型糖尿病小鼠胰腺组织中PANDER表达显著减少；2型糖尿病小鼠胰腺组织中PANDER表达明显升高.%Objective To analyze PANDER expression in pancreatic islets of type 1 and type 2 diabetic mice, and to find probe the correlationship of PANDER expression with insulin resistance in type 2 diabetic mice. Methods PANDER mRNA and protein levels were analyzed in the pancreas of STZ-induced type 1 diabetic mice, Akita diabetic mice, type 2 diabetic db/db mice. Results In the pancreas of STZ-induced and Akita diabetic mice, PANDER mRNA (STZ;1. 00 ±0.17 vs 0. 25 ±0. 06,P <0. 01; Akita: 1.00 ±0. 19 vs 0. 17 ±0. 04,P <0. 001) and protein (STZ: 1. 00 ±0. 18 vs 0. 16 ±0. 11) levels were significantly decreased when compared with non-diabetic control mice. In contrast, both PANDER mRNA (1. 00 ±0.05 vs 2. 13 ±0. 46,P < 0. 05) and protein ( 1. 00 ± 0. 28 vs 3. 58 ± 0. 36 ,P <0. 01) levels were increased in the pancreas of db/db mice as compared with db/m mice. Oral treatment of db/db mice for one month with rosiglitazone reduced pancreatic PANDER mRNA( 1.00 ±0. 13 vs 0. 28 ±0.06 ,P <0. 01) and protein expression in pancreatic islets of db/db mice, with improved insulin resistance, hyperinsu-linemia and hyperglycemia. Conclusions PANDER expression was reduced in the pancreas of type 1 diabetic mice, but was increased in the pancreas of type 2 diabetic mice.