Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

Esser, Nathalie; L’homme, Laurent; Roover, Arnaud De; Kohnen, Laurent; Scheen, André; Moutschen, Michel; Piette, Jacques; Legrand-Poels, Sylvie; Paquot, Nicolas

doi:10.1007/s00125-013-3023-9

Cited by 212 publications

(209 citation statements)

References 49 publications

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“…These data suggest that regulatory T cells may repress adipose tissue inflammation and play a role in providing protection against insulin resistance-induced inflammation linked to obesity [33,37]. The number of many other immune cells is also modified in adipose tissue during obesity and could regulate inflammation and insulin resistance [4] (Figure 1).…”

Section: Adipose Tissuementioning

confidence: 93%

“…Subcutaneous and visceral adipose tissues differ by phenotypic, physiological and functional characteristics [43]. Specific differences in inflammatory profile have also been reported, with more macrophages [29,31,33], T lymphocytes [31,33], and inflammatory molecules in the visceral vs the subcutaneous tissues of obese individuals [29,33]. Moreover, a lower number of anti-inflammatory regulatory T lymphocytes was recently found in the visceral adipose tissue of obese individuals with metabolic syndrome [33].…”

Section: Subcutaneous Versus Visceral Adipose Tissuesmentioning

confidence: 99%

“…Although it was shown that enlarged adipocytes themselves produce pro-inflammatory cytokines and chemokines [32], adipose tissue macrophages seem to be crucial for the production of adipose tissue-derived pro-inflammatory cytokines. Indeed, their recruitment correlates with the degree of obesity and is linked to systemic inflammation, insulin resistance [30] and metabolic syndrome [33]. Moreover, weight loss induced by surgery [29] or diet and exercise [10] results in a reduction in the number of adipose tissue macrophages in parallel to the decreased expression of pro-inflammatory markers in both adipose tissue and plasma of obese individuals.…”

Section: Adipose Tissuementioning

confidence: 99%

“…Obesity also induces modification in the balance between pro-inflammatory (T helper 1 and T helper 17 lymphocytes) and antiinflammatory (T helper 2 and regulatory T lymphocytes) CD4+ cells subsets, leading to secretion of cytokines from newly recruited adipose tissue macrophages [39][40][41]. Of particular interest, the number of anti-inflammatory regulatory T lymphocytes decreases with obesity in adipose tissue of both mice and humans [37,39,40] and even more in obese patients with metabolic syndrome [33]. The regulatory T lymphocytes express high amount of the antiinflammatory cytokine IL-10 which inhibit macrophage migration and induce the differentiation of M2 macrophages [35,37].…”

Section: Adipose Tissuementioning

confidence: 99%

“…Accumulating evidences also give to NLRP3 inflammasome a central role in obesity-induced insulin resistance [33,55,56]. The expression of NLRP3 inflammasome components, the activity of caspase-1 and the levels of IL-1β are increased in adipose tissue, mainly in macrophages, of obese mice and humans and directly correlate with insulin resistance, features of the metabolic syndrome and severity of T2DM [33,56].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

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Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Esser

Legrand-Poels

Piette

et al. 2014

Diabetes Research and Clinical Practice

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:It is recognized that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes. Systemic inflammatory markers are risk factors for the development of type 2 diabetes and its macrovascular complications. Adipose tissue, liver, muscle and pancreas are themselves sites of inflammation in presence of obesity. An infiltration of macrophages and other immune cells is observed in these tissues associated with a cell population shift from an anti-inflammatory to a pro-inflammatory profile. These cells are crucial for the production of pro-inflammatory cytokines, which act in an autocrine and paracrine manner to interfere with insulin signaling in peripheral tissues or induce β-cell dysfunction and subsequent insulin deficiency. Particularly, the pro-inflammatory interleukin-1β is implicated in the pathogenesis of type 2 diabetes through the activation of the NLRP3 inflammasome. The objectives of this review are to expose recent data supporting the role of the immune system in the pathogenesis of insulin resistance and type 2 diabetes and to examine various mechanisms underlying this relationship. If type 2 diabetes is an inflammatory disease, anti-inflammarory therapies could have a place in prevention and treatment of type 2 diabetes.

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Section: Adipose Tissuementioning

confidence: 93%

Section: Subcutaneous Versus Visceral Adipose Tissuesmentioning

confidence: 99%

Section: Adipose Tissuementioning

confidence: 99%

Section: Adipose Tissuementioning

confidence: 99%

Section: Accepted Manuscriptmentioning

confidence: 99%

See 3 more Smart Citations

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Esser

Legrand-Poels

Piette

et al. 2014

Diabetes Research and Clinical Practice

Self Cite

1,625

1,064

View full text Add to dashboard Cite

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Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

Burhans

Hagman

Kuzma

et al. 2018

Comprehensive Physiology

279

241

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The objective of this comprehensive review is to summarize and discuss the available evidence of how adipose tissue inflammation affects insulin sensitivity and glucose tolerance. Low-grade, chronic adipose tissue inflammation is characterized by infiltration of macrophages and other immune cell populations into adipose tissue, and a shift towards more pro-inflammatory subtypes of leukocytes. The infiltration of pro-inflammatory cells in adipose tissue is associated with an increased production of key chemokines such as C-C motif chemokine ligand 2, pro-inflammatory cytokines including tumor necrosis factor α and interleukins 1β and 6, as well as reduced expression of the key insulin sensitizing adipokine, adiponectin. In both rodent models and humans, adipose tissue inflammation is consistently associated with excess fat mass and insulin resistance. In humans, associations with insulin resistance are stronger and more consistent for inflammation in visceral as opposed to subcutaneous fat. Further, genetic alterations in mouse models of obesity that reduce adipose tissue inflammation are – almost without exception - associated with improved insulin sensitivity. However, a dissociation between adipose tissue inflammation and insulin resistance can be observed in very few rodent models of obesity as well as in humans following bariatric surgery- or low-calorie diet-induced weight loss, illustrating that the etiology of insulin resistance is multifactorial. Taken together, adipose tissue inflammation is a key factor in the development of insulin resistance and type 2 diabetes in obesity, along with other factors that likely include inflammation and fat accumulation in other metabolically active tissues.

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Increased inflammasome activity in subcutaneous adipose tissue of patients with metabolic syndrome

Pahwa

Singh

Huet

et al. 2020

Diabetes Metabolism Res

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Aims The metabolic syndrome (MetS) is an inflammatory disorder associated with an increased risk for diabetes and atherosclerotic cardiovascular disease (ASCVD). Studies in patients and animal models of obesity and diabetes have shown increased NOD‐like receptor family pyrin domain containing 3 (NLPR3) inflammasome activity. However, there is scanty data on the activity of the NLRP3 inflammasome in patients with nascent MetS. The aim of this study was to determine the status of the inflammasome in subcutaneous adipose tissue (SAT) of patients with nascent MetS without concomitant diabetes, ASCVD and smoking. Materials and Methods Patients with nascent MetS and controls were recruited from Sacramento County. Fasting blood samples were collected for biomediators of inflammation and SAT was obtained by biopsy for immunohistochemical (IHC) staining for caspase 1, IL‐1β and IL‐18. Results Caspase1, a marker of inflammasome activity and its downstream mediators IL‐1β and IL‐18 were significantly increased in SAT of patients with MetS compared to controls. Significant positive correlations of caspase 1 were obtained with certain cardio‐metabolic features, biomediators of inflammation and markers of angiogenesis and fibrosis in SAT. Both mast cell and eosinophil abundance but not macrophage density correlated with caspase1. Conclusions We make the novel observation that the SAT of patients with nascent MetS displays increased NLRP3 inflammasome activity manifest by increased caspase 1 in SAT and this may contribute to increased insulin resistance, inflammation and SAT fibrosis in these patients.

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Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

Cited by 212 publications

References 49 publications

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

Increased inflammasome activity in subcutaneous adipose tissue of patients with metabolic syndrome

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