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Chronic Exercise and Immunity
Published in James M. Rippe, Lifestyle Medicine, 2019
Melissa M. Markofski, Paul M. Coen, Michael G. Flynn
Adipose tissue macrophages are the most dominant immune cell in adipose tissue. There is evidence that adipose tissue macrophages in obese persons are more pro-inflammatory than in lean persons.23 Furthermore, activation of adipose tissue macrophages is associated with obesity and peripheral tissue insulin resistance,24 which may be abated by regular exercise. Bruun et al. reported that a 15-week hypocaloric diet and exercise intervention reduced macrophage-specific markers and inflammatory cytokines in adipose tissue.25 These effects were concomitant with improved insulin sensitivity.
Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Careful study of diet-induced obesity has identified chronic leukocyte-mediated low-grade inflammation within professional metabolic tissues as the characteristic pathophysiology of metabolic syndrome.423,427 This focus on obesity, however, has limited our understanding of leukocyte activation to the role in promoting metabolic disease. Nonetheless, leukocytes are normally present in metabolic tissues, where they perform nonredundant, supportive functions.438 In lean WAT, for example, eosinophil-derived IL-4 drives the production of IL-10 and other mediators by macrophages. This phenotype is critical for the maintenance of both adipocyte insulin sensitivity (IL-10 directly potentiates insulin signaling in adipocytes428) and the general anti-inflammatory timbre of the WAT microenvironment (both directly and through support of adipose tissue resident Treg cells).427 Congruent with these observations, disruption of IL-4 production or signaling in adipose tissue macrophages results in adipocyte dysfunction, insulin resistance, and metabolic disease.429,435,439–441 In contrast, augmentation of IL-4 signaling blunts the deleterious effects of high-fat-diet challenge.435,467
Adipose Tissue Macrophage-Mediated Inflammation in Obesity: A Link to Posttranslational Modification
Published in Immunological Investigations, 2023
Dongqin Wei, Xin Tian, Xiangyun Zhai, Chao Sun
Obesity and its comorbidities, including insulin resistance (IR), type 2 diabetes mellitus, cardiovascular disease and nonalcoholic fatty liver diseases, endanger people’s health and longevity globally (Caballero 2019). Obesity induces the recruitment of adipose tissue macrophages (ATM) and chronic low-grade inflammation. Signal communication between adipocytes and ATM is the center for regulating the occurrence and development of this inflammation (Lindhorst et al. 2021). For example, IR is not only a metabolic disorder but is also characterized by elevated inflammatory cytokine and ATM infiltration in adipose tissue (Cao et al. 2022). Although numerous studies have been performed on the crosstalk between ATM and adipocytes to induce metabolic disorders through inflammation, the root cause and mechanisms have yet to be fully elucidated. In particular, the role of posttranslational modification (PTM) is still a new research field. Therefore, the molecular crosstalk mechanism of ATM and adipocytes is discussed in the current review alongside the in-depth role of PTM.
Spotlight on liver macrophages for halting injury and progression in nonalcoholic fatty liver disease
Published in Expert Opinion on Therapeutic Targets, 2022
Tea Lund Laursen, Anders Mellemkjær, Holger Jon Møller, Henning Grønbæk, Konstantin Kazankov
Macrophages are highly active in the crosstalk between adipose tissue and the liver. Adipose tissue macrophages (ATMs) produce pro-inflammatory cytokines upholding low-grade inflammation and insulin resistance, which are key events in the development in obesity and progression of NAFLD [38,39]. On the other hand, hepatic macrophages also contribute to insulin resistance in animal models [30,34] and seem to be involved in both hepatic and peripheral insulin resistance in humans [40,41]. Besides free fatty acids and cytokines, there is an interaction between adipose tissues and hepatic macrophages through adipokines, with leptin and adiponectin being the most prominent. The levels of leptin are positively associated with the severity of disease in NAFLD, and leptin induces pro-inflammatory and pro-fibrogenic genes in hepatic macrophages, as well as stimulates HSC-dependent fibrogenesis directly [42–44]. Conversely, high levels of adiponectin may be associated with a more favorable metabolic profile in obesity [45], and adiponectin promotes macrophage tolerance to pro-inflammatory stimuli, suggesting that the positive effects of adiponectin in NAFLD may be at least partly mediated by its interaction with macrophages [46].
The effect of nutrition and exercise training on irisin and semaphorin-3E levels in obese patients
Published in Archives of Physiology and Biochemistry, 2022
Gülay Sezgin, Fatih Kar, Sema Uslu
Members of the sema-3 class have been shown to contribute to neuronal and cardiovascular morphogenesis, cancer through their effects on cell growth, survival, migration and proliferation (Zhou et al.2008). Sema-3E is upregulated in the diabetic state and sema-3e has been shown to inhibit neoangiogenesis in ischaemic tissues (Moriya et al.2010). Sema-3E expression is induced by p53 in adipocytes and allows the flow of macrophages that are derived from sema-3E monocytes into adipose tissue. These adipose tissue macrophages secrete proinflammatory mediators such as TNF-α and interleukin-6 that contribute to insulin resistance. An in vitro study demonstrates that sema-3E acting on plexin-D1 and Neuropilin-1 is a potent inducer of macrophage migration and proinflammatory cytokine expression, in addition, sema-3E inhibits insulin signalling in adipocytes by blocking Akt phosphorylation. However, these findings suggest that secretion in expanding adipose tissue supports adipocyte pathogenic functions that contribute to insulin resistance. Indeed, overexpression of Sema-3e using an adipocyte-specific promoter induced ATM deposition, insulin resistance, and glucose intolerance in mice fed a high-calorie diet. Deletion of Sema-3E improved dietary-induced adipose tissue inflammation and metabolic dysfunction (Shimizu et al.2013).