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小鼠糖尿病基因对经灌流胰岛中铷离子外流的影响。

Influence of the murine diabetes gene on rubidium ion efflux from perifused islets.

作者信息

Berglund O, Sehlin J, Täljedal I B

出版信息

Diabetologia. 1980 Jul;19(1):45-9. doi: 10.1007/BF00258310.

Abstract

Islets from diabetic C57BL/KsJ db/db mice and normal C57BL/KsJ +/+ mice were loaded with 86Rb+ and micro-perfused with nonradioactive medium for 25 min. The appearance of 86Rb+ in the effluent could be described as the sum of two exponential functions with difference proportionality constants. The rapid efflux component may have represented washout from the extracellular space, and had about the same proportionality constant in normal and diabetic mice. The slow efflux component probably reflected efflux across the islet cell plasma membranes. At 3 mmol/l D-glucose in the medium, the slow efflux was significantly retarded in diabetic as compared with normal mice. In normal mice, but not in diabetics, 20 mmol/l D-glucose inhibited the slow efflux component. It is concluded that the basal K+ permeability is decreased in KsJ db/db mouse islet cells, and that this abnormality may explain their persistant depolarization at low glucose concentrations.

摘要

将来自糖尿病C57BL/KsJ db/db小鼠和正常C57BL/KsJ +/+小鼠的胰岛用86Rb+标记,并用无放射性的培养基微灌注25分钟。流出物中86Rb+的出现可用两个具有不同比例常数的指数函数之和来描述。快速流出成分可能代表细胞外空间的洗脱,在正常和糖尿病小鼠中具有大致相同的比例常数。缓慢流出成分可能反映了跨胰岛细胞质膜的流出。在培养基中D-葡萄糖浓度为3 mmol/l时,与正常小鼠相比,糖尿病小鼠的缓慢流出明显延迟。在正常小鼠而非糖尿病小鼠中,20 mmol/l D-葡萄糖可抑制缓慢流出成分。得出的结论是,KsJ db/db小鼠胰岛细胞的基础钾通透性降低,这种异常可能解释了它们在低葡萄糖浓度下持续去极化的现象。

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