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Cited by 362

The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.

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

Southern, C., Schulster, D., Green, I.C.·1990·FEBS Letters

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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Metadata

Authors
Southern, C., Schulster, D., & Green, I. C.
Venue
FEBS Letters
Publisher
Wiley
Published
1990-12-10
Volume
276
Issue
1-2
Pages
42-44
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W1976246664
Cited by
362
References
20
FWCI
18.68
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Inhibition of insulin secretion by interleukin‐1β and tumour necrosis factor‐α via an L‐arginine‐dependent nitric oxide generating mechanism. https://app.cochat.ai/papers/10.1016/0014-5793(90)80502-a
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Southern, C., Schulster, D., & Green, I. C. (1990). Inhibition of insulin secretion by interleukin‐1β and tumour necrosis factor‐α via an L‐arginine‐dependent nitric oxide generating mechanism. FEBS Letters. https://doi.org/10.1016/0014-5793(90)80502-a

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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