INTERACTION OF BETA-CELL ACTIVITY AND IL-1 CONCENTRATION AND EXPOSURE TIME IN ISOLATED RAT ISLETS OF LANGERHANS
INTERACTION OF BETA-CELL ACTIVITY AND IL-1 CONCENTRATION AND EXPOSURE TIME IN ISOLATED RAT ISLETS OF LANGERHANS
复制标题
DOI：
10.2337/diabetes.38.10.1211
复制
发表时间：
1989-10-01
期刊：
影响因子：
7.7
通讯作者：
NERUP, J
中科院分区：
文献类型：
--
作者：
PALMER, JP;HELQVIST, S;NERUP, J
这项研究旨在检验靶细胞活动影响白介素1β的程度和时间进程的假设。(IL-1β)介导的β细胞损伤。对培养的新生大鼠胰岛进行了功能和形态的研究。细胞活动受葡萄糖和非葡萄糖试剂(15 mM L亮氨酸和10微米长效生长抑素类似物SMS201-995)的调节。在11 mM葡萄糖中，注射IL-1β2000 ng/L。导致.apprx后胰岛素释放受到抑制。在3.3 mM葡萄糖培养中，IL-1β可延迟抑制作用的开始。浓度直到暴露48小时后。类似地，L亮氨酸和SMS201-995分别刺激和抑制β细胞功能，导致IL-1β介导的抑制加速和延迟。IL-1β的量效曲线。在高β细胞活动和低β细胞活动期间，效应分别向左和向右移动。以此类推，增加IL-1β。浓度、暴露时间和β细胞活动导致胰岛解体增加。因此，静息的β细胞比工作的β细胞对IL-1β介导的节育器更具抵抗力。
This study was designed to test the hypothesis that target-cell activity influences the degree and time course of interleukin 1.beta. (IL-1.beta.)-mediated .beta.-cell impairment in vitro. Functional and morphological studies were performed in cultured newborn rat islets of Langerhans exposed from 6 h to 6 days to 50-2000 ng/L recombinant human IL-1.beta.. .BETA.-Cell activity was modulated by glucose and nonglucose agents (15 mM L-leucine and 10 .mu.M of long-acting somatostatin analogue SMS 201-995). In 11 mM glucose, 2000 ng/L of IL-1.beta. caused inhibition of insulin release after .apprx. 6 h of exposure to IL-1.beta.; in 3.3 mM glucose culture, onset of inhibition was delayed by this Il-1.beta. concentration until after 48 h of exposure. Similarly, stimulation and suppression of .beta.-cell function with L-leucine and SMS 201-995, respectively, resulted in acceleration and delay of IL-1.beta.-mediated inhibition. The dose-response curve of the IL-1.beta. effect was shifted left- and rightward during high and low .beta.-cell activity, respectively. In analogy, increasing IL-1.beta. concentration, exposure time, and .beta.-cell activity resulted in increasing islet disintegration. Thus, the resting .beta.-cell is more resistant to IL-1.beta.-mediated impariment than the working .beta.-cell.