白细胞介素-6对大鼠胰岛胰岛素分泌的抑制作用。这一作用不同于白细胞介素-1。
Inhibition of insulin secretion from rat islets of Langerhans by interleukin-6. An effect distinct from that of interleukin-1.
作者信息
Southern C, Schulster D, Green I C
机构信息
Department of Biochemistry, School of Biological Sciences, University of Sussex, Brighton, U.K.
出版信息
Biochem J. 1990 Nov 15;272(1):243-5. doi: 10.1042/bj2720243.
Abstract
Glucose-induced insulin secretion from islets cultured in the presence of interleukin-6 (IL-6) for 12-24 h was inhibited to a similar extent as when islets were treated with interleukin-1 beta (IL-1 beta). However, unlike IL-1 beta, IL-6 did not potentiate insulin secretion during an acute (30 min) exposure of islets to the cytokine, nor did it inhibit DNA synthesis during a 24 h culture period. A 12 h pretreatment of islets with tumour necrosis factor-alpha (TNF-alpha) combined with IL-1 beta potentiated the inhibitory effect of IL-1 beta on secretion, such that 20 mM-glucose-induced insulin secretion was abolished. No synergistic inhibition of secretion was observed with TNF-alpha and IL-6. However, IL-1 beta and IL-6 were found to inhibit insulin secretion in an additive manner. These results suggest that IL-6 inhibits insulin secretion in a manner distinct from that of IL-1 beta, and that IL-6 is unlikely to mediate the inhibitory effects of IL-1 beta or TNF-alpha on rat islets of Langerhans.
摘要
在白细胞介素-6（IL-6）存在的情况下培养12至24小时的胰岛，其葡萄糖诱导的胰岛素分泌受到的抑制程度与用白细胞介素-1β（IL-1β）处理胰岛时相似。然而，与IL-1β不同的是，在胰岛急性（30分钟）暴露于该细胞因子期间，IL-6不会增强胰岛素分泌，在24小时培养期内也不会抑制DNA合成。用肿瘤坏死因子-α（TNF-α）与IL-1β对胰岛进行12小时预处理，可增强IL-1β对分泌的抑制作用，使得20 mM葡萄糖诱导的胰岛素分泌被消除。未观察到TNF-α与IL-6对分泌的协同抑制作用。然而，发现IL-1β和IL-6以相加的方式抑制胰岛素分泌。这些结果表明，IL-6以不同于IL-1β的方式抑制胰岛素分泌，并且IL-6不太可能介导IL-1β或TNF-α对大鼠胰岛的抑制作用。
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