摘要
目的探讨胰高糖素样肽（ＧＬＰ）－１（７－３６）ＮＨ_２促胰岛素分泌的机制。方法以 Ｆｌｕｏ－３为探针，用粘附式细胞仪研究 ＧＬＰ－ １（７－ ３６）ＮＨ_２对培养的新生大鼠胰岛β细胞内游离 Ｃａ^（２＋）浓度的作用。结果在 ２．８ ｍｍｏｌ／Ｌ葡萄糖时，ＧＬＰ－ １（７－ ３６）ＮＨ_２不能使胰岛 β细胞内游离 Ｃａ^（２＋）升高，而优降糖使β细胞内游离 Ｃａ^（２＋）升高明显。在 １６．７ ｍｍｏｌ／Ｌ葡萄糖时，ＧＬＰ－１（７－３６）ＮＨ_２使胰岛β细胞内Ｃａ^（２＋）升高明显，ＥＧＴＡ和硝苯吡啶能完全阻滞ＧＬＰ－１（７－３６）ＮＨ_２引起的Ｃａ^（２＋）升高。结论ＧＬＰ－１（７－３６）ＮＨ_２具有葡萄糖浓度依赖的促胰岛素释放作用，细胞外Ｃａ^（２＋）通过电压依赖性钙通道内流对其引起的β细胞内游离Ｃａ^（２＋）升高起重要作用。
Objective To explore the mechanisms by which GLP- l(7 - 36)NH_2 stimulates insulin release. Methods Using adherent cell analysis and sorting cytometer (ACAS) with Fluo - 3 as a probe, effect of glucagon - like peptidc - 1 (7 - 36)NH_2 on cytoplasmic Ca^(2+) concentalion was investigated in cultured neonatal rat pancreatic islst β - Cells. Results In the presence of 2. 8 mmol/ L glucose, GLP - 1 (7 - 36)NH_2 had no effect on cytoplasmic Ca^(2+) in β - Cells, but glybenclamide increased in cytoplasmic Ca^(2)+ in β- Cells. In the presence of 16.7 mmol/L glucose,GLP- l(7 - 36)NH_2 produced a marked increase in cytoplasmic Ca^(2+) in β - cells, which was completely inhibited by EGTA or nifedipine. Conclusion GLP - 1 (7 - 36) NH_2 can stimulate insulin release in a glucose concentration- dependent manner. Inflax of Ca^(2+) through voltage - dependent L - type Ca^(2+) channels plays an important role in increasing cytoplasmic Ca^(2+) in β - cells.
出处
《广东医学》
CAS
CSCD
2000年第4期286-288,共3页
Guangdong Medical Journal
