Mechanisms of obesity and related pathology: linking immune responses to metabolic stress

Abstract

There is a tightly regulated interaction, which is well‐conserved in evolution, between the metabolic and immune systems that is deranged in states of over‐ or under‐nutrition. Obesity, an energy‐rich condition, is characterized by the activation of an inflammatory process in metabolically active sites such as adipose tissue, liver and immune cells. The consequence of this response is a sharp increase in circulating levels of proinflammatory cytokines, adipokines and other inflammatory markers. Activation of the immune response in obesity is mediated by specific signaling pathways, with Jun N‐terminal kinase and IκB kinase β/nuclear factor κ‐light‐chain‐enhancer of activated B cells being the most well studied. It is known that the above events modify insulin signaling and result in the development of insulin resistance. The nutrient overload characterizing obesity is a metabolic stressor associated with intracellular organelle (e.g. the endoplasmic reticulum) stress. The exact characterization of the series of events and the mechanisms that integrate the inflammatory response with metabolic homeostasis at the cellular and systemic level is a very active research field. In this minireview, we discuss the signaling pathways and molecules associated with the development of obesity‐induced inflammation, as well as the evidence that supports a critical role for the stress response in this process.

Effect of acute and regular exercise on growth hormone secretagogue receptor-1a expression in human lymphocytes, T cell subpopulation and monocytes

“…There is increasing evidence of the coupling of immune status to the metabolic system (Dixit and Taub, 2005;Karalis et al, 2009;Odegaard and Chawla, 2013). This communication is mediated via a complex array of cytokines, hormones and neuropeptides.…”

Pleural fluid analysis of lung cancer vs benign inflammatory disease patients

“…p27, Skp2, Cox2, CycD1 and Ki67 are considered as tumour and/or proliferation markers (Huang et al, 2003;Siggelkow et al, 2004;Adjei, 2005;Vig-Varga et al, 2006;Garg et al, 2008;Park et al, 2008;Chang et al, 2009;Meeran et al, 2009;Mukhopadhyay et al, 2009), ImAnOx and carbonyls are oxidative markers (Nyström, 2005;Bahar et al, 2007) and MMP-9, -3 and -2 are MMPs that are expressed in various pathological processes such as inflammation and cancer and also in response to infections (Korpos et al, 2009;Oikonomidi et al, 2009;Vanlaere and Libert, 2009). Enhanced oxidative stress characterises both inflammation and cancer; all other markers analysed were also shown previously to be associated with inflammation, as well as with oxidative stress, presumably mediated through the activation of NF-kB (Huang et al, 2003;Vig-Varga et al, 2006;Park et al, 2008;Gonda et al, 2009;Karalis et al, 2009;Ku et al, 2009;Perricone et al, 2009;Víctor et al, 2009). Interestingly, the significantly altered markers correlated among themselves ( Table 2), indicating that they were all associated with each other, prompting hypothesis that they might belong to a single biological network that, when fully understood, may be used for the development of drugs related to lung cancer.…”

Selected Innate Immune System Response to Aerobic Exercise Training in Obese Down Syndrome Children

“…Many previous studies like Moulin et al, showed in their study that obesity is associated with alteration in immune system parameters [18]. A state of chronic inflammation and increased count of WBCs, monocytes and neutrophils have been reported in obese individuals [19][20][21][22]. Also, an elevated number of lymphocytes, macrophages, CD3 and CD4 have been found to be positively correlated with the body mass index [23,24].…”