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FEBS Lett. 1990 Dec 10;276(1-2):42-4.

Inhibition of insulin secretion by interleukin-1 beta and tumour necrosis factor-alpha via an L-arginine-dependent nitric oxide generating mechanism.

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1
Department of Biochemistry, University of Sussex, Brighton, UK.

Abstract

Inhibition of glucose-induced insulin secretion by interleukin-1 beta (IL-1 beta), or IL-1 beta plus tumour necrosis factor-alpha (TNF-alpha), 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-1 beta was further alleviated when islets were maintained in L-arginine-free medium supplemented with N-omega-nitro-L-arginine methyl ester (NAME), while synergism between IL-1 beta plus TNF-alpha was completely abolished. Tissue culture medium nitrite levels were raised in islets treated with IL-1 beta or TNF-alpha (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-1 beta, and accounts for the phenomenon of synergism between IL-1 beta and TNF-alpha.

PMID:
2265709
DOI:
10.1016/0014-5793(90)80502-a
[Indexed for MEDLINE]
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