Tilg M, Moschen ARAdipocytokines: mediators linking adipose tissue, inflammtion and immunity. Nat Rev Immunol 6:772-783

Christian Doppler Research Laboratory for Gut Inflammation and Department of Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
Nature reviews. Immunology (Impact Factor: 34.99). 11/2006; 6(10):772-83. DOI: 10.1038/nri1937
Source: PubMed


There has been much effort recently to define the role of adipocytokines, which are soluble mediators derived mainly from adipocytes (fat cells), in the interaction between adipose tissue, inflammation and immunity. The adipocytokines adiponectin and leptin have emerged as the most abundant adipocyte products, thereby redefining adipose tissue as a key component not only of the endocrine system, but also of the immune system. Indeed, as we discuss here, several adipocytokines have a central role in the regulation of insulin resistance, as well as many aspects of inflammation and immunity. Other adipocytokines, such as visfatin, have only recently been identified. Understanding this rapidly growing family of mainly adipocyte-derived mediators might be of importance in the development of new therapies for obesity-associated diseases.

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Available from: Alexander R Moschen, Apr 04, 2014
    • "Various products of the adipose tissue and liver have been characterized including cytokines such as adiponectin, leptin, resistin, visfatin, RBP4, TNF-α, IL-6, IL-1, IL-18 and fetuin-A [16]. Adiponectin is one of key adipokines regulating insulin signaling, inflammation, as well as glucose and lipid metabolism in adipose tissue and liver [30] [31]. Adiponectin is negatively associated with the pro-inflammatory cytokines TNF-α and IL-6 [32,33], and down-regulates these cytokines by suppressing the activation of Kupffer cells and hepatic stellate cells as well as by attenuating the translocation of NF-κB to the nucleus [34]. "
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    ABSTRACT: Metabolic homeostasis is maintained by the coordinated regulation of several physiological processes and organ crosstalk. Especially, the interaction between adipose tissue and liver is critical for the regulation of glucose and lipid metabolism. This study investigated the involvement of resveratrol (RSV) in the crosstalk between adipokine adiponectin and hepatokine fetuin-A. Adipocytes-hepatocytes co-culture system and a high-fat (HF) diet-induced obesity (DIO) mouse model were utilized. Protein levels of adiponectin and fetuin-A were analyzed in adipocytes and hepatocytes with the knockdown of adiponectin and fetuin-A, respectively. After six weeks of the HF diet treatment, RSV was delivered via an osmotic pump for four weeks. The experimental groups were lean control fed with a standard diet, HF diet-induced obese control and HF_RSV (8 mg/kg/day). After 4 weeks of each treatment, blood and tissues were collected, and the levels of adiponectin and fetuin-A were analyzed. RNA interference during co-culture of adipocytes and hepatocytes demonstrated the existence of crosstalk between adiponectin and fetuin-A. The four-week RSV treatment resulted in increased serum adiponectin and decreased serum fetuin-A in diet-induced obesity mice. The serum levels of adiponectin and fetuin-A were inversely related. In epididymal fat depots, RSV increased adiponectin, peroxisome proliferator-activated receptor (PPAR) alpha, PPAR gamma, sirtuin1 and AMP-activated protein kinase (AMPK). RSV lowered fetuin-A and NF-κB, and increased liver AMPK. These results demonstrate the crosstalk between adiponectin and fetuin-A, and suggest that RSV may be involved in adipose tissue and liver crosstalk through the interaction between adiponectin and fetuin-A. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jul 2015 · The Journal of nutritional biochemistry
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    • "Excess energy is mostly stored as adipocyte in the adipose tissue, resulting in obesity. It is well known that obesity is a major source of cytokines and other factors being secreted from adipocytes [1] [2], which causes adversity in the body. However, recent studies have reported that adipose tissues secrete large amount of hormones that regulate appetite and energy homeostasis, and thus interest has been refocused on these tissues as being the key factor to perform important endocrine functions [1] [3]. "
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    ABSTRACT: The purpose of this study was to investigate the effect of regular treadmill exercise on the mRNA expressions of myokines and angiogenesis factors in the skeletal muscle of obese rats. Thirty two male Sprague-Dawley rats (4weeks old) were divided into the CO (control) and HF (high fat diet) groups. Obesity was induced in the HF group by consumption of 45% high-fat diet for 15 weeks. These groups were further subdivided into training groups (COT and HFT); the training groups conducted moderate intensity treadmill training for 8 weeks. Soleus muscles were excised and analyzed by real-time quantitative PCR. mRNA expression of myokines, such as PGC-1α, IL-6, and IL-15, in the COT and HFT groups (which conducted regular exercise), were higher as compared with the CO and HF groups (p < 0.05). Also, the levels in the HF group were significantly lower when compared with CO group (p < 0.05). Expression of angiogenesis mRNA, namely mTOR, VEGF, and FLT1, were significantly lower in the HF group, as compared to the CO group (p < 0.05). In addition, COT group had a higher expression of mTORC1, mTORC2, VEGF and FLT mRNA, than the CO group (p < 0.05); the HFT group also had higher expressions of mTOR, VEGF and FLT1 mRNA than the HF group (p < 0.05). These results indicate that mRNA expression of myokines was increased through the activity of muscle contraction, and it also promoted the mRNA expression of angiogenesis due to activation of mTOR. Thus, we conclude that not only under normal health conditions, but in obesity and excess nutritional circumstances also, regular exercise seems to act positively on the glycemic control and insulin sensitivity through the angiogenesis signaling pathway.
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    • "TNF-a stimulates angiogenesis and, in combination with other proinflammatory cytokines, can provoke alterations in endothelial cells leading to several pathologies involving the microvasculature. Given its involvement as a master regulator of other inflammatory cytokines, TNF-a has been postulated to be the most important cytokine in the pathogenesis of IMIDs [4], including autoimmune diseases, insulin resistance, and cancer [5]. There is evidence to suggest that chronic inflammation has a pathological role in obesity and type 2 diabetes (T2D). "
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    ABSTRACT: Condensed polycyclic heteroaromatic cations bearing a bridgehead nitrogen with pyridazino[1' ,6':1,2]pyrido[3,4-b]indolinium and pyridazino[1,6-a]benzimidazolium structures were assayed as inhibitors of LPS-induced TNF-alpha production by THP-1 cells. The hit compound 1e, which had the best IC50 value (4.49 micromolar) and low toxicity, was further assayed on human PMBCs (IC50 3.91 micromolar) and monocytes (IC50 1.82 micromolar). This compound also inhibited TNF-alpha production following poly I:C stimulation of humanmonocytes and monocyte-derived dendritic cells; in the latter case, inhibition of IL-12 production was also observed. Compound 1e was also able to inhibit TNF-alpha expression at the transcriptional level and proved to be effective in vivo. Compound 1e is an interesting potential therapeutic agent in IMIDs.
    Full-text · Article · May 2015 · European Journal of Medicinal Chemistry
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