Editorials |
From the Kidney Research Centre, University of Ottawa, Ontario, Canada.
Correspondence to Rhian M. Touyz, MD, PhD, Canada Research Chair in Hypertension, Kidney Research Centre, OHRI/University of Ottawa, Room 303, 451 Smyth Rd, Ottawa, K1H 8M5. E-mail rtouyz@uottawa.ca
See related article, pages 12451252
Key Words: inflammation adipokines interleukin endothelium TNF-
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Adipose tissue is no longer considered an inert energy storage tissue, but an active participant contributing to physiological and pathological processes associated with inflammation, immunity, appetite, insulin sensitivity, endocrine and reproductive systems, bone metabolism, and endothelial function.1,2 Adipose tissue synthesizes and secretes proinflammatory and antiinflammatory metabolically- and hormonally-active substances, collectively called adipokines or adipocytokines and include leptin, adiponectin, resistin, and visfatin.3,4 Adipose tissue also produces cytokines and chemokines, such as tissue necrosis factor (TNF)-1
, interleukin (IL)-1ß, IL-6, IL-8, IL-10, transforming growth factor (TGF)-ß, nerve growth factor and the acute-phase response plasminogen activator inhibitor-1, haptoglobin, and serum amyloid.1,2,5 Although adipose tissue produces various polypeptide and non-protein factors, only leptin, adiponectin, resistin, adipsin, and visfatin are primarily synthesized by adipocytes.3,4 Whereas leptin plays a role mainly in appetite regulation,6 resistin induces insulin resistance and is proinflammatory7 whereas visfatin acts as an insulin-mimetic and is antiapoptotic.8
Of all the adipokines, adiponectin is found in highest concentrations in the circulation.9 It is secreted specifically from adipocytes and it regulates insulin sensitivity.10 Low serum levels are causally linked to insulin resistance, obesity, and type 2 diabetes and are predictive for development of diabetes and cardiovascular disease.11,12 Obesity is associated with decreased adiponectin levels, and adiponectin is now being considered a putative therapeutic agent in the management of obesity.13,14 Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice.15,16 Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes.17,18 This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through
Related Article:
Circ. Res. 2005 97: 1245-1252.
This article has been cited by other articles:
![]() |
N. G. Abraham and A. Kappas Pharmacological and Clinical Aspects of Heme Oxygenase Pharmacol. Rev., March 1, 2008; 60(1): 79 - 127. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2005 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |