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

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Abstract
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.

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