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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    • "Although a comprehensive functional description for resistance in humans is still to be determined, its proinflammatory properties indicate an important role in inflammatory processes. Visfatin is an adipokine that is secreted by visceral fat adipocytes and decreases insulin sensitivity [56] [91]. There are significant positive relationships between visceral visfatin expression and BMI, percent body fat, and waist circumference [87]. "
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    ABSTRACT: Objectives: Obesity is a significant quality of life-impairing health problem affecting industrialized nations. However, despite carrying a large fat mass, some very obese individuals exhibit normal metabolic profiles (metabolically healthy obesity). The physiological factors underlying their protective and favorable metabolic profiles remain poorly defined. Methods: A search of the National Library of Medicine PubMed database was performed using the following keywords: Metabolically healthy obese, metabolically normal obese, insulin resistance, metabolically unhealthy normal weight, and uncomplicated obesity. Results: This article reviewed factors associated with severe obesity that lacks complications, and suggests putative activities by which these obese individuals avoid developing the clinical features of metabolic syndrome, or the metabolic complications associated with severe obesity. Conclusions: Despite the knowledge that visceral fat deposition is the seminal factor that ultimately causes insulin resistance (IR) and the detrimental inflammatory and hormonal profile that contributes to increase risk for cardiovascular disease, it remains unknown whether metabolically healthy obesity (MHO) has genetic predisposing factors, and whether MHO ultimately succumbs to IR and the metabolic syndrome, indicating a need for prophylatic bariatric surgery.
    Nutrition 10/2015; DOI:10.1016/j.nut.2015.07.010 · 2.93 Impact Factor
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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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