PANCREATIC-ISLET CELLS - EFFECTS OF MONOSACCHARIDES, GLYCOLYTIC INTERMEDIATES AND METABOLIC-INHIBITORS ON MEMBRANE-POTENTIAL AND ELECTRICAL-ACTIVITY
PANCREATIC-ISLET CELLS - EFFECTS OF MONOSACCHARIDES, GLYCOLYTIC INTERMEDIATES AND METABOLIC-INHIBITORS ON MEMBRANE-POTENTIAL AND ELECTRICAL-ACTIVITY
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DOI：
10.1113/jphysiol.1975.sp010899
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发表时间：
1975-01-01
影响因子：
5.5
通讯作者：
SAKAMOTO, Y
中科院分区：
文献类型：
--
作者：
DEAN, PM;MATTHEWS, EK;SAKAMOTO, Y
1.使用单个细胞内微电极进行电压记录和电流注入，研究了单糖、糖酵解中间体、代谢抑制剂和安夏对体外小鼠胰岛细胞膜电活性的影响。2.除了D-葡萄糖（28 mM）、D-甘露糖（16- 6 mM）和L-亮氨酸（10 mM）外，D-甘油醛（11 mM）和乙酰乙酸（20 mM）物质也能诱导胰岛细胞的动作电位，但其他葡萄糖类似物和代谢中间体（包括L-葡萄糖）不能。3.甘露庚酮糖（20 mM），而不是D-半乳糖或2-脱氧-D-葡萄糖，拮抗由D-葡萄糖（28 mM）诱导的胰岛细胞电活动。 先前用甘露庚酮糖处理细胞导致它们过度兴奋，并完全防止随后暴露于D-葡萄糖时出现电活动。4.当细胞同时暴露于D-葡萄糖和抑制剂时，由D-葡萄糖28 mM诱导的电活动可被根皮苷10 mM进行性抑制，并在用抑制剂预处理30-60 min时被消除。根皮苷还引起胰岛细胞的去极化，这与细胞外葡萄糖无关。5.缺氧完全阻断葡萄糖诱导的电活动，但不能阻断D-甘油醛、L-亮氨酸、甲苯磺丁脲或格列本脲诱发的电活动。6.碘乙酸（5 mM）可快速阻断葡萄糖诱导的电活动，而甲苯磺丁脲引起的电活动对抑制作用具有相对抗性。7.在胰岛细胞中的葡萄糖受体的性质和可能的位置进行了讨论的葡萄糖诱导的电活动和胰岛素分泌的起源和功能意义。
1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro‐electrode for both voltage recording and current injection. 2. In addition to D‐glucose (28mM), D‐mannose (16–6mM), and L‐leucin (10mM), the substances D‐glyceraldehyde (11mM), and acetoacetate (20 mM), induced action potentials in islet cells but other glucos analogues and metabolic intermediates including L‐glucose dod not. 3. Mannoheptulose 20 mM), but not D‐galactose or 2‐deoxy‐D‐glucose, antagonized the electrical activity induced in islet cells by D‐glucose, 28mM. Prior treatment of the cells with mannoheptulose caused them to hyperpolarize and completely prevented the appearance of electrical activity on subsequent exposure to D‐glucose. 4. Electrical activity induced by D0glucose 28mM, was progressively inhibited by phloridzin, 10mM, if the cells were exposed to D‐glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30–60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose. 5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D‐glyceraldehyde, L‐leucine, tolbutamide or glibenclamide. 6. Iodoacetic acid, 5 mM, rapidly blocked glucose‐induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic islet cells is discussed in relation to the origin and functional significance of glucose‐induced electrical activity and insulin secretion.