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机构地区:[1]广州军区广州总医院内分泌科,510010 [2]第一军医大学南方医院内分泌科,510515
出 处:《广东医学》2000年第4期286-288,共3页Guangdong Medical Journal
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.
关 键 词:胰岛素 胰岛Β细胞 游离钙 GLP-1(7-36)NH2
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