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Cited by 960

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase

Open access
Talukdar, Saswata, Oh, Da Young, Bandyopadhyay, Gautam, Li, Dongmei, Xu, Jianfeng, McNelis, Joanne, Lu, Min, Li, Pingping, Yan, Qingyun, Zhu, Yimin, Ofrecio, Jachelle, Lin, Michael, Brenner, Martin B, Olefsky, Jerrold M·2012·Nature Medicine
DOI 10.1038/nm.2885
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Abstract

Chronic low-grade adipose tissue and liver inflammation is a major cause of systemic insulin resistance and is a key component of the low degree of insulin sensitivity that exists in obesity and type 2 diabetes. Immune cells, such as macrophages, T cells, B cells, mast cells and eosinophils, have all been implicated as having a role in this process. Neutrophils are typically the first immune cells to respond to inflammation and can exacerbate the chronic inflammatory state by helping to recruit macrophages and by interacting with antigen-presenting cells. Neutrophils secrete several proteases, one of which is neutrophil elastase, which can promote inflammatory responses in several disease models. Here we show that treatment of hepatocytes with neutrophil elastase causes cellular insulin resistance and that deletion of neutrophil elastase in high-fat-diet–induced obese (DIO) mice leads to less tissue inflammation that is associated with lower adipose tissue neutrophil and macrophage content. These changes are accompanied by improved glucose tolerance and increased insulin sensitivity. Taken together, we show that neutrophils can be added to the extensive repertoire of immune cells that participate in inflammation-induced metabolic disease.

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Crossref · 10.1038/nm.2885

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Metadata

Authors
Talukdar, S., Oh, D. Y., Bandyopadhyay, G., Li, D., Xu, J., McNelis, J., Lu, M., Li, P., Yan, Q., Zhu, Y., Ofrecio, J., Lin, M., Brenner, M. B., & Olefsky, J. M.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2012-08-05
Volume
18
Issue
9
Pages
1407-1412
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
DOI
10.1038/nm.2885
OpenAlex
W2053142936
Cited by
960
References
9
FWCI
46.96
Type
journal article
Language
en
Open access
green

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