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Circulation Research. 2005;96:1042-1052
doi: 10.1161/01.RES.0000165803.47776.38
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(Circulation Research. 2005;96:1042.)
© 2005 American Heart Association, Inc.


Review

Adipocyte Signaling and Lipid Homeostasis

Sequelae of Insulin-Resistant Adipose Tissue

Yi-Hao Yu, Henry N. Ginsberg

From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY.

Correspondence to Henry N. Ginsberg, MD, Department of Medicine, PH 10–305, Columbia University College of Physicians and Surgeons, 630 West 168th St, New York, NY 10032. E-mail hng1{at}columbia.edu

This Review is part of a thematic series on Adipocyte Signaling in the Cardiovascular System, which includes the following articles:

Adipose Tissue, Inflammation and Cardiovascular Disease
Adipocyte Signaling and Lipid Homeostasis: Sequelae of Insulin Resistant Adipose Tissue
Diabetic Cardiomyopathy: The Search for a Unifying Hypothesis
Adipocyte Signaling and the Vasculature
PPARgamma Activation and Effects on the Vasculature

Phillip Scherer Guest Editor

For many years adipose tissue was viewed as the site where excess energy was stored, in the form of triglycerides (TGs), and where that energy, when needed elsewhere in the body, was released in the form of fatty acids (FAs). Recently, it has become clear that when the regulation of the storage and release of energy by adipose tissue is impaired, plasma FA levels become elevated and excessive metabolism of FA, including storage of TGs, occurs in nonadipose tissues. Most recently, work by several laboratories has made it clear that in addition to FA, adipose tissue communicates with the rest of the body by synthesizing and releasing a host of secreted molecules, collectively designated as adipokines. Several recent reviews have described how these molecules, along with FA, significantly effect total body glucose metabolism and insulin sensitivity. Relatively little attention has been paid to the effects of adipokines on lipid metabolism. In this review, we will describe, in detail, the effects of molecules secreted by adipose tissue, including FA, leptin, adiponectin, resistin, TNF-{alpha}, IL-6, and apolipoproteins, on lipid homeostasis in several nonadipose tissues, including liver, skeletal muscle, and pancreatic ß cells.


Key Words: lipids • fatty acids • adipose tissue • insulin resistance • cytokines




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