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glucose metabolism, hepatic steatosis, pancreatic characteristics and the associated inflammation were analysed. Materials and methods Mice and diets Animal care was in accordance with institutional guidelines and the 2010/63/EU directive from the European

Introduction Inflammation is part of the body’s innate immune response and is an essential process that not only defends against harmful bacteria and pathogens but also plays a key role in the maintenance and repair of tissues. It is mediated

increased mortality not only from vascular disease but also from complications of cirrhosis and hepatocellular cancer. Thus, targeting hepatocellular inflammation is expected to significantly prevent the progression of the disease and reduce mortality in

presumed to be due, in part, to lack of a reliable animal model. Because inflammation is a hallmark of AAA, we induced an inflammatory AAA murine model in wild-type mice by modification of our previous finding ( Son et al. 2015 ). Using this AAA model

assertion made by the WHO that no progress will be made in the management of preterm labour until we understand the processes involved in human labour. Myometrial inflammation is held to play a key role in the onset of labour, repressing progesterone

Metabolic injury and hepatocytes There are several intra- as well as extrahepatic triggers for inflammation in NASH that relate to the metabolic injury to the liver ( Schuster et al. 2018 ). While this review does not aim to provide a detailed overview

Introduction Obesity is widely considered as a state with low-grade chronic inflammation ( de Heredia et al. 2012 ). Elevated circulating levels of inflammatory cytokines, such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-6

inflammation and hyperglycemia (this manuscript). Because microbes can directly infect adipocytes and induce systemic inflammation and metabolic dysregulation ( Schäffler & Schölmerich 2010 ), and given the well-established link between adipose tissue

inflammation ( Yamashita et al . 2007 , den Besten et al . 2015 , Jin et al . 2015 ). Indeed, SCFAs, mainly acetate, propionate, and butyrate, are not only metabolic substrates, but also signaling molecules that regulate metabolism ( Koh et al . 2016

the alleviation of inflammation stems from the inhibition of nuclear factor kappa B-driven inflammation ( Manna & Aggarwal 1998 , Yang et al. 2015 ). Melanocortin activation reduces the expression of proinflammatory cytokines, their receptors and