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1
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本文引用的文献

1
Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans.强啡肽对离体大鼠胰岛中胰岛素和生长抑素分泌、钙摄取及环磷酸腺苷水平的影响。
Diabetes. 1983 Aug;32(8):685-90. doi: 10.2337/diab.32.8.685.
2
Effects of pregnancy in the rat on the size and insulin secretory response of the islets of Langerhans.大鼠妊娠对胰岛大小及胰岛素分泌反应的影响。
J Endocrinol. 1972 Aug;54(2):317-25. doi: 10.1677/joe.0.0540317.
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Potassium ions and the secretion of insulin by islets of Langerhans incubated in vitro.钾离子与体外培养的胰岛分泌胰岛素的关系。
Biochem J. 1968 Jun;108(1):17-24. doi: 10.1042/bj1080017.
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Low concentrations of interleukin-1 stimulate and high concentrations inhibit insulin release from isolated rat islets of Langerhans.
Acta Endocrinol (Copenh). 1986 Dec;113(4):551-8. doi: 10.1530/acta.0.1130551.
5
Human tumor necrosis factor potentiates human interleukin 1-mediated rat pancreatic beta-cell cytotoxicity.人肿瘤坏死因子增强人白细胞介素1介导的大鼠胰腺β细胞细胞毒性。
J Immunol. 1987 Dec 15;139(12):4077-82.
6
Inhibitory effects of interleukin 1 on insulin secretion, insulin biosynthesis, and oxidative metabolism of isolated rat pancreatic islets.白细胞介素1对离体大鼠胰岛胰岛素分泌、胰岛素生物合成及氧化代谢的抑制作用。
Endocrinology. 1987 Oct;121(4):1424-31. doi: 10.1210/endo-121-4-1424.
7
Destruction of rat islet cell monolayers by cytokines. Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin, and interleukin 1.细胞因子对大鼠胰岛细胞单层的破坏作用。γ干扰素、肿瘤坏死因子、淋巴毒素和白细胞介素1的协同相互作用。
Diabetes. 1988 Jan;37(1):133-6. doi: 10.2337/diab.37.1.133.
8
Multiple actions of interleukin 6 within a cytokine network.白细胞介素6在细胞因子网络中的多种作用。
Immunol Today. 1988 May;9(5):137-9. doi: 10.1016/0167-5699(88)91200-5.
9
Descriptive and mechanistic considerations of interleukin 1 and insulin secretion.
Diabetes. 1988 Oct;37(10):1311-5. doi: 10.2337/diab.37.10.1311.
10
Evidence for IL-6 production by and effects on the pancreatic beta-cell.白细胞介素-6由胰腺β细胞产生及对其产生影响的证据。
J Immunol. 1989 Aug 15;143(4):1188-91.

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.

DOI:10.1042/bj2720243
PMID:2264829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1149683/
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。