CYCLIC-AMP POTENTIATES GLUCOSE-INDUCED INSULIN RELEASE FROM MOUSE PANCREATIC-ISLETS WITHOUT INCREASING CYTOSOLIC FREE CA-2+
CYCLIC-AMP POTENTIATES GLUCOSE-INDUCED INSULIN RELEASE FROM MOUSE PANCREATIC-ISLETS WITHOUT INCREASING CYTOSOLIC FREE CA-2+
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DOI：
10.1111/j.1748-1716.1985.tb07766.x
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发表时间：
1985-01-01
期刊：
影响因子：
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通讯作者：
ABRAHAMSSON, H
中科院分区：
文献类型：
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作者：
RORSMAN, P;ABRAHAMSSON, H
RORSMAN P. & ABRAHAMSSON, H. 1985。环 AMP 增强葡萄糖诱导的小鼠胰岛胰岛素释放，而不增加胞质游离 Ca2+。Acta Physiol Scand125, 639–647。 1985 年 3 月 18 日收稿，1985 年 5 月 28 日接受。ISSN 0001–6772。瑞典乌普萨拉大学生物医学系医学细胞生物学系。使用指示剂 quin-2 研究了各种胰岛素释放刺激剂对分散培养的 ob/ob 小鼠胰腺 β 细胞中胞质游离 Ca2+ ([Ca2+]i) 的影响，该指示剂本身对葡萄糖诱导的胰岛素释放和糖代谢只有轻微影响。静息 [Ca2+]i 为 158 ± 7 nM。将葡萄糖增加至 20 mM 后，[Ca2+] 逐渐上升之前有 1-2 分钟的滞后期，5-6 分钟后达到高出 60% 的新平台。通过添加毛喉素增加细胞内环 AMP 不会进一步增加 [Ca2+]i；相反，尽管胰岛素分泌加倍，但暂时略有减少。高细胞外 K+ 引起去极化后，胞质 [Ca2+] 显着增加，这表明 β 细胞功能的维持。此外，二丁酰环 AMP 和茶碱缺乏将 [Ca2+]i 升高到超过葡萄糖所获得的能力。结果表明，环 AMP 通过使分泌机制对 [Ca2+] 的变化敏感而不是通过增加离子的胞质浓度来增强葡萄糖诱导的胰岛素释放。
RORSMAN P. & ABRAHAMSSON, H. 1985. Cyclic AMP potentiates glucose‐induced insulin release from mouse pancreatic islets without increasing cytosolic free Ca2+.Acta Physiol Scand125, 639–647. Received 18 March 1985, accepted 28 May 1985. ISSN 0001–6772. Department of Medical Cell Biology, Biomedicum, University of Uppsala, Sweden.The effects of various stimulants of insulin release on cytosolic free Ca2+, [Ca2+]i, in dispersed and cultured pancreatic β‐cells fromob/ob‐mice were studied using the indicator quin‐2, which in itself has only slight effects on the glucose‐induced insulin release and the metabolism of the sugar. The resting [Ca2+]iwas 158 ± 7 nM. After increasing glucose to 20 mM there was a lag‐period of 1–2 min before [Ca2+]igradually rose, reaching a new plateau 60% higher after 5–6 min. Increasing intracellular cyclic AMP by adding forskolin did not further increase [Ca2+]i; on the contrary there was a slight temporary reduction despite a doubling of insulin secretion. The maintenance of the β‐cell function was evident from a marked increase of cytosolic [Ca2+]iafter depolarization evoked by high extracellular K+. Also dibutyryl cyclic AMP and theophylline lacked the ability to raise [Ca2+]ibeyond that obtained by glucose. The results suggest that cyclic AMP potentiates glucose‐induced insulin release by sensitizing the secretory machinery to changes of [Ca2+]irather than by increasing the cytosolic concentration of the ion.