The glycation of immunoreactive insulin (IRI) was assessed in extracts of pancreas and islets from control and hyperglycemic animal models. Glycated and nonglycated IRI were separated by affinity chromatography and quantified by radioimmunoassay. Hydrocortisone-treated Wistar rats (80 mg x kg-1 x day-1 and obese hyperglycemic (ob/ob) mice showed significant increases in plasma glucose (P < 0.001), percentage glycated hemoglobin (P < 0.001), plasma IRI (P < 0.01), and total pancreatic IRI content (P < 0.01), compared with their respective controls. These diabetic groups also demonstrated significant increases (P < 0.05) in the percentage of glycated pancreatic IRI above the controls. Streptozotocin-treated (200 mg/kg) Swiss TO mice exhibited significant increases in plasma glucose (P < 0.001), glycated hemoglobin (P < 0.001), and percentage glycated pancreatic IRI (P < 0.05), compared with untreated controls, despite a marked decrease in both plasma IRI (P < 0.001) and total pancreatic IRI content (P < 0.001). Significant elevations in the percentage of glycated IRI were also observed in islets isolated from obese hyperglycemic (ob/ob) mice (P < 0.001), compared with islets from lean controls, and when lean mouse islets were cultured in hyperglycemic media for 24 h (33.3 vs. 5.6 mmol/l D-glucose; P < 0.001). The contribution of glycated plus nonglycated insulin and proinsulin to the total IRI was estimated in lean and obese mouse pancreatic extracts following high-performance liquid chromatography separation. The contribution of proinsulin to the total IRI was approximately 10%. Proinsulin represented 27-28% of the total glycated IRI. These data indicate that the glycation of insulin and proinsulin occurs within the pancreatic islets and is elevated in both insulin-deficient and insulin-resistant diabetic animal models.

译文

在对照和高血糖动物模型的胰腺和胰岛提取物中评估了免疫反应性胰岛素 (IRI) 的糖基化。通过亲和色谱分离糖化和非糖化IRI,并通过放射免疫分析法进行定量。氢化可的松处理的Wistar大鼠 (80 mg × kg-1 × day-1) 和肥胖高血糖 (ob/ob) 小鼠的血浆葡萄糖 (P <0.001),糖化血红蛋白百分比 (P <0.001),血浆IRI (P <0.01),和胰腺IRI总含量 (P <0.01),与他们各自的对照组相比,这些糖尿病组的糖化胰腺IRI的百分比也显著增加 (P <0.05),高于对照组。链脲佐菌素治疗 (200 mg/kg) Swiss对小鼠的血浆葡萄糖显著增加 (P <0.001),与未治疗的对照组相比,糖化血红蛋白 (P < 0.001) 和糖化胰腺IRI百分比 (P <0.05),尽管血浆IRI (P < 0.001) 和总胰腺IRI含量 (P < 0.001) 均显著降低。与瘦肉对照组的胰岛相比,从肥胖高血糖 (ob/ob) 小鼠分离的胰岛 (P < 0.001) 中也观察到糖化IRI的百分比显著升高,当瘦鼠胰岛在高血糖培养基中培养24 h (33.3 vs. 5.6 mmol/l D-葡萄糖; P <0.001)。在高效液相色谱分离后,估计了瘦瘦和肥胖小鼠胰腺提取物中糖化加非糖化胰岛素和胰岛素原对总IRI的贡献。胰岛素原对总IRI的贡献约为10%。胰岛素原占总糖化IRI的27-28%。这些数据表明胰岛素和胰岛素原的糖基化发生在胰岛内,并且在胰岛素缺乏和胰岛素抵抗的糖尿病动物模型中均升高。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录