Adipokines in inflammation and metabolic disease. Nat Rev Immunol

Department of Molecular Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho Showa-ku, Nagoya, 466-8550 Japan.
Nature Reviews Immunology (Impact Factor: 34.99). 02/2011; 11(2):85-97. DOI: 10.1038/nri2921
Source: PubMed


The worldwide epidemic of obesity has brought considerable attention to research aimed at understanding the biology of adipocytes (fat cells) and the events occurring in adipose tissue (fat) and in the bodies of obese individuals. Accumulating evidence indicates that obesity causes chronic low-grade inflammation and that this contributes to systemic metabolic dysfunction that is associated with obesity-linked disorders. Adipose tissue functions as a key endocrine organ by releasing multiple bioactive substances, known as adipose-derived secreted factors or adipokines, that have pro-inflammatory or anti-inflammatory activities. Dysregulated production or secretion of these adipokines owing to adipose tissue dysfunction can contribute to the pathogenesis of obesity-linked complications. In this Review, we focus on the role of adipokines in inflammatory responses and discuss their potential as regulators of metabolic function.

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    • "The NGF is secreted by rat, mice and human BAT (Nisoli et al., 1996) and also by WAT in mice (Peeraully et al., 2004), where its expression and secretion were related to the role of the neurotrophin in the inflammatory response. It is known that accumulation of fat could lead to a state of chronic mild inflammation (Ouchi et al., 2011), as demonstrated by granulocytic infiltration and cytokine secretion in AT (Osborn and Olefsky, 2012). An infiltration of macrophages into different AT depots was not observed after calving (Akter et al., 2012), but later in lactation, an infiltration of immune cells could occur. "
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    ABSTRACT: Currently, there are no reports of neurotrophins in adipose tissue of cows. The distribution of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and their high-affinity tyrosine kinase receptors TrkA and TrkB, was investigated by immunohistochemical method in the subcutaneous adipose tissue of cow at mid-lactation. Results revealed the localization of NGF and BDNF along the plasma membrane and cytoplasm of adipocytes. Neurotrophin receptors TrkA and TrkB showed moderate and strong positive staining in adipocytes, respectively. The expression of NGF, BDNF, TRKB — but not of TRKA — was also confirmed at transcriptional level by RT-PCR analyses. Considering the involvement of BDNF on fat metabolism and of NGF on activation of the sympathetic response in human and rodents, these neurotrophins could be related to lipogenesis and lipolysis occurring during lactation in cows. The local production of these neurotrophins supports their potential paracrine function for the regulation of adipocyte activity and deserve further investigations.
    Research in Veterinary Science 08/2015; 102:196-199. DOI:10.1016/j.rvsc.2015.08.016 · 1.41 Impact Factor
    • "After excess dietary nutrient uptake (or decreased energy expenditure), WAT can take up both glucose and free fatty acids from blood plasma to be converted to triglycerides; however in humans reesterification of fatty acids occurs preferentially compared with de novo lipogenesis from glucose [11]. WAT is in turn able to alter nutritional status by the release of adipokines into the vasculature and lymphatic systems , including leptin, adiponectin, resistin, and the inflammatory mediators TNF-␣ and IL-6 [12] [13]. In the context of obesity, these play both local (adipocyte proliferation and differentiation ) and central roles (controlling satiety and energy catabolism). "
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    ABSTRACT: There are two types of adipose tissue with distinct functions - white adipose tissue (WAT) stores chemical energy as triglycerides, whereas brown adipose tissue (BAT) consumes energy and releases heat (thermogenesis) in response to sympathetic nerve activity. In humans, treatments that promote greater BAT deposition and/or activity would be highly beneficial in regimes aimed at reducing obesity. Adult humans have restricted populations of prototypical brown adipocytes in the neck and chest areas, but recent advances have established that adipocytes with similar properties, termed "brite" adipocytes, can be recruited in subcutaneous depots thought to be primarily WAT. These brite adipocytes express the protein machinery required for thermogenesis, but to assess brite adipocytes as viable therapeutic targets, we need to understand how to promote conversion of white adipocytes to brite adipocytes and ways to increase optimal energy consumption and thermogenesis in these brite adipocytes. This can be accomplished by pharmacological and nutritional therapies to differing degrees, as reviewed in detail here. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500251 · 4.60 Impact Factor
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    • "Inflammatory state of adipose tissue alters the type and level of adipokines produced. Anti-inflammatory adipokines promote insulin sensitivity and pro-inflammatory adipokines promote insulin resistance (Juge-Aubry et al., 2005; Ouchi et al., 2011). Excess secretion of pro-inflammatory adipokines aggravates endothelial dysfunction, inflammation in liver, muscle, brain; the tissues that are critical for regulation of energy and food metabolism (Kwon and Pessin, 2013; Conde et al., 2011). "
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    ABSTRACT: Adipose tissue secretes adipokines that regulate insulin sensitivity in adipocytes and other peripheral tissues critical to glucose metabolism. Insulin resistance is associated with severe alterations in adipokines characterized by release of increased pro-inflammatory cytokines and decreased anti-inflammatory cytokines from adipose tissue. The role of Farnesoid X receptor (FXR) activation on adipokines in relation to adipose tissue inflammation and insulin resistance is not completely explored. For the first time, we have evaluated the ability of Chenodeoxycholic acid (CDCA), an endogenous FXR ligand, in restoring the disturbance in adipokine secretion and insulin resistance in palmitate treated 3T3-L1 cells and adipose tissues of High fat diet (HFD) rats. CDCA suppressed several of the tested pro-inflammatory adipokines (TNF-α, MCP-1, IL-6, Chemerin, PAI, RBP4, resistin, vaspin), and enhanced the major anti-inflammatory and insulin sensitizing adipokines (adiponectin, leptin). CDCA suppressed the activation of critical inflammatory regulators such as NF-κB and IKKβ which are activated by palmitate treatment in differentiated cells and HFD in rats. We show the altered adipokines in insulin resistance, its association with inflammatory regulators, and the role of CDCA in amelioration of insulin resistance by modulation of adipokines. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Molecular and Cellular Endocrinology 07/2015; 414:19-28. DOI:10.1016/j.mce.2015.07.012 · 4.41 Impact Factor
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