Adipose Inflammation in Obesity: Relationship With Circulating Levels of Inflammatory Markers and Association With Surgery-Induced Weight Loss

Lasselin, Julie; Magne, Eric; Beau, Cédric; Ledaguenel, Patrick; Dexpert, Sandra; Aubert, Agnès; Layé, Sophie; Capuron, Lucile

doi:10.1210/jc.2013-2673

Cited by 81 publications

(55 citation statements)

References 37 publications

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“…This finding is consistent with the known ability of adipose tissue in obese individuals to elaborate inflammatory cytokines, potentially mimicking similar properties of leukocytes. 34 At the same time, as shown in Fig. 5, DNA methylation in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI.…”

Section: Discussionmentioning

confidence: 70%

Epigenome-wide profiling of DNA methylation in paired samples of adipose tissue and blood

et al. 2016

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Many epigenetic association studies have attempted to identify DNA methylation markers in blood that are able to mirror those in target tissues. Although some have suggested potential utility of surrogate epigenetic markers in blood, few studies have collected data to directly compare DNA methylation across tissues from the same individuals. Here, epigenomic data were collected from adipose tissue and blood in 143 subjects using Illumina HumanMethylation450 BeadChip array. The top axis of epigenome-wide variation differentiates adipose tissue from blood, which is confirmed internally using cross-validation and externally with independent data from the two tissues. We identified 1,285 discordant genes and 1,961 concordant genes between blood and adipose tissue. RNA expression data of the two classes of genes show consistent patterns with those observed in DNA methylation. The discordant genes are enriched in biological functions related to immune response, leukocyte activation or differentiation, and blood coagulation. We distinguish the CpG-specific correlation from the within-subject correlation and emphasize that the magnitude of within-subject correlation does not guarantee the utility of surrogate epigenetic markers. The study reinforces the critical role of DNA methylation in regulating gene expression and cellular phenotypes across tissues, and highlights the caveats of using methylation markers in blood to mirror the corresponding profile in the target tissue.

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Section: Discussionmentioning

confidence: 70%

Epigenome-wide profiling of DNA methylation in paired samples of adipose tissue and blood

et al. 2016

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“…Conversely, weight loss, induced either by low-caloric diet or bariatric surgery, significantly reduces peripheral inflammation in obese individuals (Belza et al, 2009;Hakeam et al, 2009;Manco et al, 2007;Rao, 2012) and animals (Liu et al, 2014;Schneck et al, 2014;Zhang et al, 2011). Adipocytes, together with infiltrated macrophages and T cells that progressively accumulate in the white adipose tissue, have indeed the ability to potently secrete inflammatory mediators (Cancello et al, 2006;Gregor and Hotamisligil, 2011;Kim et al, 2014;Lasselin et al, 2014b;Zeyda et al, 2011). Part of systemic inflammation in obesity also comes from other organs, in particular, the liver and muscles that are similarly infiltrated by activated immune cells (McNelis and Olefsky, 2014;Pedersen and Febbraio, 2012).…”

Section: Is Inflammation Linking Fat To Depression?mentioning

confidence: 99%

“…Similar effects have been reported following chronic psychosocial stress, which induces both inflammation and metabolic alterations, including weight gain (Bierhaus et al, 2003;Chuang et al, 2010;Kleinridders et al, 2009). Interestingly, obesity-associated inflammation, notably as it relates to the visceral adipose tissue, was found to impact obesity treatment outcomes, with increased adipose expression of immune cells and inflammatory markers being associated with lower BMI reduction after bariatric surgery in severely obese patients (Lasselin et al, 2014b). In addition to the hypothalamus, the hippocampus and cortex also display signs of neuroinflammation in rodent models of obesity (Dinel et al, 2011(Dinel et al, , 2014Erion et al, 2014;Pistell et al, 2010).…”

Section: Is Inflammation Linking Fat To Depression?mentioning

confidence: 99%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

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141

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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“…Obesity has profound effects on immunity and inflammation being critical contributors to the pathogenesis of these metabolic disorders (Esser et al 2014;Klöting and Blüher 2014;Lumeng and Saltiel 2011). In this sense, white blood cell counts (Dixon and O'Brien 2006;Vozarova et al 2002) as well as plasma levels of acute-phase proteins (Gómez-Ambrosi et al 2006;Yudkin et al 1999) and pro-inflammatory cytokines (Catalán et al 2007a;Lasselin et al 2014) are elevated in obese and T2D patients experimenting a reduction after weight loss (Bastard et al 2000;Catalán et al 2011). The obesity-associated low-grade inflammation results in the persistent stimulation of the immune system mainly characterized by the infiltration of adipose tissue with macrophages (Poulain-Godefroy et al 2008;Weisberg et al 2003) and the activation of circulating immune cells shifting toward a pro-inflammatory profile (Ghanim et al 2004;Lumeng et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

et al. 2015

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Inflammation is a critical contributor to the pathogenesis of metabolic disorders with adipose tissue being crucial in the inflammatory response by releasing multiple adipokines with either pro-or anti-inflammatory activities with potential functions as metabolic regulators. Peripheral blood mononuclear cells (PBMC) have been proposed as representative of the inflammatory status in obesity. The aim of the present study was to evaluate the contribution of PBMC to the obesity-associated chronic inflammation analyzing the expression of novel adipokines. Samples obtained from 69 subjects were used in the study. Real-time PCR determinations were performed to quantify gene expression levels in PBMC of novel adipokines including chemerin, chitinase-3-like protein 1 (YKL-40), lipocalin-2 (LCN-2) and osteopontin (OPN), and their circulating concentrations were also determined by ELISA. We show, for the first time, that PBMC gene expression levels of chemerin (P \ 0.0001), chitinase-3-like protein 1 (P = 0.010), lipocalin-2 (P \ 0.0001) and osteopontin (P \ 0.0001) were strongly upregulated in obesity independently of the glycemic state. Circulating concentrations of these adipokines followed the same trend being significantly higher (P \ 0.05) in obese normoglycemic and type 2 diabetic patients compared to lean volunteers and also associated (P \ 0.05) with their corresponding mRNA levels in PBMC. These results provide evidence that alterations in inflammation-related adipokines are manifest in PBMC, which might contribute to the low-grade chronic inflammation that characterizes obesity.

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Adipose Inflammation in Obesity: Relationship With Circulating Levels of Inflammatory Markers and Association With Surgery-Induced Weight Loss

Abstract: These findings support the involvement of macrophages and T cells in adipose inflammation and provide new information regarding the role of the visceral adipose tissue in the inflammatory state of obesity and its impact on obesity treatment outcomes, such as surgery-induced weight loss.

Cited by 81 publications

References 37 publications

Epigenome-wide profiling of DNA methylation in paired samples of adipose tissue and blood

Epigenome-wide profiling of DNA methylation in paired samples of adipose tissue and blood

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

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