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Cited by 1,199

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Tumor necrosis factor alpha inhibits signaling from the insulin receptor.

Open access
Hotamisligil, G S, Murray, D L, Choy, L N, Spiegelman, B M·1994·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.91.11.4854
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Abstract

Insulin resistance is a common problem associated with infections and cancer and, most importantly, is the central component of non-insulin-dependent diabetes mellitus. We have recently shown that tumor necrosis factor (TNF) alpha is a key mediator of insulin resistance in animal models of non-insulin-dependent diabetes mellitus. Here, we investigate how TNF-alpha interferes with insulin action. Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. The IR isolated from TNF-alpha-treated cells is also defective in the ability to autophosphorylate and phosphorylate IR substrate 1 in vitro. These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin.

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Crossref · 10.1073/pnas.91.11.4854

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Metadata

Authors
Hotamisligil, G. S., Murray, D. L., Choy, L. N., & Spiegelman, B. M.
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1994-05-24
Volume
91
Issue
11
Pages
4854-4858
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.91.11.4854
OpenAlex
W2022930571
Cited by
1,199
References
3
FWCI
20.67
Type
journal article
Language
en
Open access
bronze

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