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Iyad H Manaserh, Emily Maly, Marziyeh Jahromi, Lakshmikanth Chikkamenahalli, Joshua Park, and Jennifer Hill

activated by cold exposure, by high fat diets, and after meal consumption ( Vosselman et al. 2013 ), a phenomenon known as postprandial thermogenesis. Changes in thermoregulation can result in dysregulation of the systemic metabolism ( Heeren & Munzberg

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Juliane K Czeczor, Amanda J Genders, Kathryn Aston-Mourney, Timothy Connor, Liam G Hall, Kyoko Hasebe, Megan Ellis, Kirstie A De Jong, Darren C Henstridge, Peter J Meikle, Mark A Febbraio, Ken Walder, and Sean L McGee

from the amyloidogenic and non-amyloidogenic processing of APP could have different effects on aspects of systemic metabolism ( Czeczor & McGee 2017 ). Studies in neuronal cells have suggested that the AICD peptide derived from amyloidogenic

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Mark A Exley, Laura Hand, Donal O'Shea, and Lydia Lynch

Obesity is a major risk factor for metabolic disease, with white adipose tissue (WAT) inflammation emerging as a key underlying pathology. Alongside its major role in energy storage, WAT is an important endocrine organ, producing many bioactive molecules, termed adipokines, which not only serve as regulators of systemic metabolism, but also possess immunoregulatory properties. Furthermore, WAT contains a unique immune cell repertoire, including an accumulation of leukocytes that are rare in other locations. These include alternatively activated macrophages, invariant natural killer T cells, and regulatory T cells. Disruption of resident adipose leukocyte homeostasis contributes to obesity-associated inflammation and consequent metabolic disorder. Despite many recent advances in this new field of immuno-metabolism, fundamental questions of why and how inflammation arises as obesity develops are not yet fully understood. Exploring the distinct immune system of adipose tissue is fundamental to our understanding of the endocrine as well as immune systems. In this review, we discuss the roles of adipose tissue leukocytes in the transition to obesity and progression of inflammation and highlight potential anti-inflammatory therapies for combating obesity-related pathology.

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Clara Lefranc, Malou Friederich-Persson, Roberto Palacios-Ramirez, and Aurelie Nguyen Dinh Cat

Obesity is a multifaceted, chronic, low-grade inflammation disease characterized by excess accumulation of dysfunctional adipose tissue. It is often associated with the development of cardiovascular (CV) disorders, insulin resistance and diabetes. Under pathological conditions like in obesity, adipose tissue secretes bioactive molecules called ‘adipokines’, including cytokines, hormones and reactive oxygen species (ROS). There is evidence suggesting that oxidative stress, in particular, the ROS imbalance in adipose tissue, may be the mechanistic link between obesity and its associated CV and metabolic complications. Mitochondria in adipose tissue are an important source of ROS and their dysfunction contributes to the pathogenesis of obesity-related type 2 diabetes. Mitochondrial function is regulated by several factors in order to preserve mitochondria integrity and dynamics. Moreover, the renin–angiotensin–aldosterone system is over-activated in obesity. In this review, we focus on the pathophysiological role of the mineralocorticoid receptor in the adipose tissue and its contribution to obesity-associated metabolic and CV complications. More specifically, we discuss whether dysregulation of the mineralocorticoid system within the adipose tissue may be the upstream mechanism and one of the early events in the development of obesity, via induction of oxidative stress and mitochondrial dysfunction, thus impacting on systemic metabolism and the CV system.

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Å Tivesten, E Bollano, H C Nyström, C Alexanderson, G Bergström, and A Holmäng

results may be partly explained by the complexity of sex steroid biology, including local and systemic metabolism of sex steroids. Testosterone is readily aromatized into oestradiol (E 2 ), and 5α-reduced into the more potent and non-aromatizable androgen

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Joan Villarroya, Rubén Cereijo, Aleix Gavaldà-Navarro, Marion Peyrou, Marta Giralt, and Francesc Villarroya

) relative to those with just thermogenic impairment of BAT (e.g. UCP1-null mice) ( Lowell et al. 1993 ); second, the widespread observations that the experimental transplantation of small amounts of BAT lead to relevant effects on systemic metabolism

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Margo P Emont, Hui Yu, and Jun Wu

regulates both brown and beige fat function. We also discuss the effects that thermogenic fat activation may have on systemic metabolism in humans, and highlight molecules that have begun to be tested as drug targets. Transcriptional control of

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Sheree D Martin and Sean L McGee

effects on systemic metabolism ( Samuel & Shulman 2012 ). With respect to glucose metabolism, insulin resistance impairs the suppression of hepatic glucose output by failing to adequately inhibit glycogenolysis. Simultaneously, glucose uptake and disposal

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Terese M Zidon, Jaume Padilla, Kevin L Fritsche, Rebecca J Welly, Leighton T McCabe, Olivia E Stricklin, Aaron Frank, Youngmin Park, Deborah J Clegg, Dennis B Lubahn, Jill A Kanaley, and Victoria J Vieira-Potter

’s beneficial role in systemic metabolism in aged mice; however, those authors did not assess ERβ’s role. Since selective agonization of ERα is not recommended in postmenopausal women who have an elevated risk for breast cancer, our findings that ERβ may also

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Aijun Zhang, Douglas H Sieglaff, Jean Philippe York, Ji Ho Suh, Stephen D Ayers, Glenn E Winnier, Alexei Kharitonenkov, Christopher Pin, Pumin Zhang, Paul Webb, and Xuefeng Xia

carbohydrate metabolism ( Table 4 ). Inspection of these relationships did not allow us to generate many obvious predictions about the influences of these genes upon local hepatic and systemic metabolism (see ‘Discussion’). Table 3 IPA canonical pathway