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Fat as an endocrine organ: Relationship to the metabolic syndrome

Published on Dec 1, 2005in The American Journal of the Medical Sciences1.962
· DOI :10.1097/00000441-200512000-00005
Louise J. Hutley15
Estimated H-index: 15
(UQ: University of Queensland),
John Prins59
Estimated H-index: 59
(UQ: University of Queensland)
Abstract
Obesity and the metabolic syndrome have both reached pandemic proportions. Together they have the potential to impact on the incidence and severity of cardiovascular pathologies, with grave implications for worldwide health care systems. The metabolic syndrome is characterized by visceral obesity, insulin resistance, hypertension, chronic inflammation, and thrombotic disorders contributing to endothelial dysfunction and, subsequently, to accelerated atherosclerosis. Obesity is a key component in development of the metabolic syndrome and it is becoming increasingly clear that a central factor in this is the production by adipose cells of bioactive substances that directly influence insulin sensitivity and vascular injury. In this paper, we review advances in the understanding of biologically active molecules collectively referred to as adipokines and how dysregulated production of these factors in obese states mediates the pathogenesis of obesity associated metabolic syndrome.
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References188
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Recently, visfatin was characterized as a novel adipocytokine that is upregulated in obesity and exerts insulinmimetic effects in various tissues. To clarify expression and regulation of this adipocytokine, visfatin mRNA was measured by quantitative real-time reverse transcriptionpolymerase chain reaction in 3T3-L1 adipocytes during adipogenesis and after treatment with various hormones known to alter insulin sensitivity. Visfatin expression was about 6-fold higher in 3T3-L1 adipocytes in vitro ...
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