Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2276-2283
Published online before print September 6, 2007, doi: 10.1161/ATVBAHA.107.147835
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
27/11/2276    most recent
ATVBAHA.107.147835v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gustafson, B.
Right arrow Articles by Smith, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gustafson, B.
Right arrow Articles by Smith, U.
Related Collections
Right arrowRelated Article
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2276.)
© 2007 American Heart Association, Inc.


Brief Reviews

Inflamed Adipose Tissue

A Culprit Underlying the Metabolic Syndrome and Atherosclerosis

Birgit Gustafson; Ann Hammarstedt; Christian X. Andersson; Ulf Smith

From the The Lundberg Laboratory for Diabetes Research, Center of Excellence for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.

Correspondence to Dr Ulf Smith, The Lundberg Laboratory for Diabetes Research, Center of Excellence for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. E-mail ulf.smith{at}medic.gu.se

Series Editor: Marja-Riitta Taskinen

The metabolic syndrome is associated with a dysregulated adipose tissue; in part a consequence of adipose cell enlargement and the associated infiltration of macrophages. Adipose cell enlargement leads to a proinflammatory state in the cells with reduced secretion of adiponectin and with increased secretion of several cytokines and chemokines including interleukin (IL)-6, IL-8, and MCP-1. MCP-1 has been shown to play an important role for the associated recruitment of macrophages into the adipose tissue. The increased release of cytokines leads to an impaired differentiation of the preadipocytes with reduced lipid accumulation and induction of adiponectin, thus promoting ectopic lipid storage. In particular tumor necrosis factor (TNF) {alpha}, but also IL-6, has been shown to induce these effects in preadipocytes and this is associated with an increased Wnt signaling maintaining the cells in an undifferentiated and proinflammatory state. The proinflammatory state in the adipose tissue also leads to a local insulin resistance including an impaired inhibitory effect of insulin on FFA release. The insulin resistance further supports the proinflammatory state because insulin, by itself, is both antilipolytic and antiinflammatory by antagonizing cytokine-induced activation of STAT signaling.

The Metabolic Syndrome is associated with a dysregulated adipose tissue attributable to inflammation with increased levels of several proinflammatory molecules. This alters the pattern of adipokines produced and prevents the differentiation of preadipocytes. Furthermore, insulin resistance is induced which enhances both lipolysis and the proinflammatory state because insulin has antiinflammatory effects.


Key Words: adipose tissue • cytokines • insulin • thiazolidinediones • insulin resistance


Related Article:

Is Metabolic Syndrome the Main Threat to Human Health in the Twenty-First Century?
Marja-Riitta Taskinen
Arterioscler. Thromb. Vasc. Biol. 2007 27: 2275. [Full Text] [PDF]



This article has been cited by other articles:


Home page
J Am Coll CardiolHome page
J. Sanz, P. R. Moreno, and V. Fuster
The year in atherothrombosis.
J. Am. Coll. Cardiol., March 4, 2008; 51(9): 944 - 955.
[Full Text] [PDF]