Inhibition of insulin secretion by interleukin‐1β and tumour necrosis factor‐α via an L‐arginine‐dependent nitric oxide generating mechanism

FEBS Letters

Green, I.C.¹  Southern, C.¹  Schulster, D.² 

[1]Department of Biochemistry, University of Sussex, Brighton, BN1 9QG, UK

[2]National Institute for Biological Standards and Controls, Herts, EN6 3QG, UK

关键词: Interleukin-1β;    Tumour necrosis factor-α;    L-Arginine;    Nitric oxide;    Insulin secretion;    Rat;   

DOI  :  10.1016/0014-5793(90)80502-A

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Inhibition of glucose-induced insulin secretion by interleukin-1β (IL-1β), or IL-1β plus tumour necrosis factor-α (TNF-α), was less marked when rat islets of Langerhans were cultured for 12 h with these cytokines in L-arginine-free medium as opposed to medium containing L-arginine (1 mM). Inhibition of secretion by IL-1β was further alleviated when islets were maintained in L-arginine-free medium supplemented with N-ω-nitro-L-arginine methyl ester (NAME), while synergism between IL-1β plus TNF-α was completely abolished. Tissue culture medium nitrite levels were raised in islets treated with IL-1β or TNF-α (48 h). Cytokine-stimulated nitrite production was not observed in islets cultured with NAME (1 mM). In conclusion, an L-arginine-dependent nitric oxide generating mechanism is involved in the inhibition of insulin secretion by IL-1β, and accounts for the phenomenon of synergism between IL-1β and TNF-α.

【 授权许可】

Unknown