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Signalling role of adipose tissue: adipokines and inflammation in obesity

Trayhurn, P., Wood, I.S.·2005·Biochemical Society Transactions

Abstract

White adipose tissue (WAT) is a major endocrine and secretory organ, which releases a wide range of protein signals and factors termed adipokines. A number of adipokines, including leptin, adiponectin, tumour necrosis factor α, IL-1β (interleukin 1β), IL-6, monocyte chemotactic protein-1, macrophage migration inhibitory factor, nerve growth factor, vascular endothelial growth factor, plasminogen activator inhibitor 1 and haptoglobin, are linked to inflammation and the inflammatory response. Obesity is characterized by a state of chronic mild inflammation, with raised circulating levels of inflammatory markers and the expression and release of inflammation-related adipokines generally rises as adipose tissue expands (adiponectin, which has anti-inflammatory action is an exception). The elevated production of inflammation-related adipokines is increasingly considered to be important in the development of diseases linked to obesity, particularly Type II diabetes and the metabolic syndrome. WAT is involved in extensive cross-talk with other organs and multiple metabolic systems through the various adipokines.

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Cites

Show all 15 references

Research works printed but not linked: 30

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Metadata

Authors
Trayhurn, P., & Wood, I. S.
Venue
Biochemical Society Transactions
Published
2005-10-26
Volume
33
Issue
5
Pages
1078-1081
ISSN
  • 0300-5127 (ISSN-L)
  • 1470-8752
OpenAlex
W2071926369
Cited by
588
References
15
FWCI
21.38
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Signalling role of adipose tissue: adipokines and inflammation in obesity. https://app.cochat.ai/papers/10.1042/bst0331078
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Trayhurn, P., & Wood, I. S. (2005). Signalling role of adipose tissue: adipokines and inflammation in obesity. Biochemical Society Transactions. https://doi.org/10.1042/bst0331078

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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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