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Review
. 2008 Nov;93(11 Suppl 1):S64-73.
doi: 10.1210/jc.2008-1613.

Adipocytokines and the metabolic complications of obesity

Affiliations
Review

Adipocytokines and the metabolic complications of obesity

Neda Rasouli et al. J Clin Endocrinol Metab. 2008 Nov.

Abstract

Context: Adipose tissue is increasingly recognized as an active endocrine organ with many secretory products and part of the innate immune system. With obesity, macrophages infiltrate adipose tissue, and numerous adipocytokines are released by both macrophages and adipocytes. Adipocytokines play important roles in the pathogenesis of insulin resistance and associated metabolic complications such as dyslipidemia, hypertension, and premature heart disease.

Evidence acquisition: Published literature was analyzed with the intent of addressing the role of the major adipose secretory proteins in human obesity, insulin resistance, and type 2 diabetes.

Evidence synthesis: This review analyzes the characteristics of different adipocytokines, including leptin, adiponectin, pro-inflammatory cytokines, resistin, retinol binding protein 4, visfatin, and others, and their roles in the pathogenesis of insulin resistance.

Conclusions: Inflamed fat in obesity secretes an array of proteins implicated in the impairment of insulin signaling. Further studies are needed to understand the triggers that initiate inflammation in adipose tissue and the role of each adipokine in the pathogenesis of insulin resistance.

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Figures

Figure 1
Figure 1
Role of TSP1, TGF-β, and PAI-1 in adipose tissue. TSP1 is expressed by adipose tissue, and activates TGF-β, which in turn activates PAI-1, which is a procoagulant. TGF-β is also activated by high glucose and angiotensin II. TSP1 expression is inhibited by PPARγ agonists, which may explain some of the beneficial effects of these drugs.
Figure 2
Figure 2
Changes in adipose tissue, liver, and muscle with obesity and insulin resistance. The adipose tissue of lean subjects contains few macrophages, and secretes relatively high levels of adiponectin, and low levels of inflammatory cytokines. β-Oxidation of lipids in muscle is high, and there is little ectopic fat in the muscle and liver. With obesity and insulin resistance, adipose tissue contains many macrophages, and the tissue secretes high levels of many adipokines, and low levels of adiponectin. This adipose tissue may be limited in its lipid storage capacity, and this feature, along with the pro-inflammatory state, promotes ectopic lipid accumulation. The adipose tissue in some subjects can be characterized as expandable, meaning the tissue can accommodate more lipid. This may result from treatment with a TZD. Such adipose tissue may be less inflamed, and because this adipose tissue can accumulate more lipid, there is less ectopic fat.

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