. 2010 , Younossi et al . 2011 ). It is histologically characterized by hepatic triglyceride (TG) accumulation of more than 5%, resulting in steatosis and hepatic inflammation ( Tarantino et al . 2010 ). NAFLD includes a complex spectrum of disorders
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Mohamed Asrih and François R Jornayvaz
A Boelen, J Kwakkel, W M Wiersinga, and E Fliers
increased hypothalamic interleukin (IL)-1β mRNA expression ( Boelen et al. 2004 ). It is known that chronic inflammation in mice, induced by an s.c. injection of turpentine in each hind limb also results in altered peripheral thyroid hormone metabolism
L E Nicol, W F Grant, S M Comstock, M L Nguyen, M S Smith, K L Grove, and D L Marks
tissue inflammation driven by innate immune responses to longstanding exposure to gluco- and lipotoxicity. Such chronic and ongoing insults manifesting as auto-inflammation are now recognized as part of obesity-related metabolic disease and are associated
Sandra K Szlapinski, Anthony A Botros, Sarah Donegan, Renee T King, Gabrielle Retta, Brenda J Strutt, and David J Hill
). Clinical studies have shown that glucose intolerance after parturition involves β-cell dysfunction ( Buchanan & Xiang 2005 , Retnakaran et al. 2008 , Xiang et al. 2010 , Molęda et al. 2013 ) which can occur, in part, due to inflammation and
Shisan Xu, Fangjing Xie, Li Tian, Samane Fallah, Fatemeh Babaei, Sinai H C Manno, Francis A M Manno III, Lina Zhu, Kin Fung Wong, Yimin Liang, Rajkumar Ramalingam, Lei Sun, Xin Wang, Robert Plumb, Lee Gethings, Yun Wah Lam, and Shuk Han Cheng
test, * P < 0.05, n = 5~6. Figure 5 Estrogen induces inflammation in the injured zebrafish heart. A. Gene Ontogeny (GO) terms significantly enriched in genes differentially expressed in female vs male hearts at 7 dpc, n = 3. (B
Caroline Davidge-Pitts, Carlos J Escande, and Cheryl A Conover
circulating cytokines, chemokines, and growth factors ( Lacasa et al . 2007 ). This adipose tissue inflammation leads to a higher likelihood of adverse metabolic profiles, including diabetes and atherosclerosis, particularly in subjects with visceral fat
P Delerive, JC Fruchart, and B Staels
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily. PPARalpha is highly expressed in liver, skeletal muscle, kidney, heart and the vascular wall. PPARgamma is predominantly detected in adipose tissue, intestine and macrophages. PPARs are activated by fatty-acid derivatives and pharmacological agents such as fibrates and glitazones which are specific for PPARalpha and PPARgamma respectively. PPARs regulate lipid and lipoprotein metabolism, glucose homeostasis, cell proliferation and differentiation, and apoptosis. PPARalpha controls intra- and extracellular lipid metabolisms whereas PPARgamma triggers adipocyte differentiation and promotes lipid storage. In addition, PPARs also modulate the inflammatory response. PPAR activators have been shown to exert anti-inflammatory activities in various cell types by inhibiting the expression of proinflammatory genes such as cytokines, metalloproteases and acute-phase proteins. PPARs negatively regulate the transcription of inflammatory response genes by antagonizing the AP-1, nuclear factor-kappaB (NF-kappaB), signal transducer and activator of transcription and nuclear factor of activated T-cells signalling pathways and by stimulating the catabolism of proinflammatory eicosanoids. These recent findings indicate a modulatory role for PPARs in inflammation with potential therapeutical applications in chronic inflammatory diseases.
Silvia Tapia-Gonzalez, Paloma Carrero, Olga Pernia, Luis M Garcia-Segura, and Yolanda Diz-Chaves
oestradiol may be exerted by reducing brain inflammation acting on microglia. Oestradiol has been shown to inhibit the expression of inflammatory mediators by microglia in vitro ( Bruce-Keller et al . 2000 , 2001 , Drew & Chavis 2000, Vegeto et al
Stephanie R Thorn, Stig Purup, Mogens Vestergaard, Kris Sejrsen, Matthew J Meyer, Micheal E Van Amburgh, and Yves R Boisclair
and IGF-I (e.g. insulin receptor substrate-proteins (IRS) proteins; Rui et al . 2002 , Wellen & Hotamisligil 2005 ). Adipose tissue expansion also induces the production of other proteins associated with inflammation, including transforming growth
Philip Newsholme, Vinicius Cruzat, Frank Arfuso, and Kevin Keane
resulting in glucolipotoxicity (for further details, see review Newsholme et al . (2012 b ) )). Excessive ROS can activate key inflammation pathways including nuclear factor κ-light-chain-enhancer of activated B cells (NFκB) and c-Jun NH 2 -terminal kinase
