Chemerin as a Mediator between Obesity and Vascular Inflammation in Children

Landgraf, Kathrin; Friebe, Daniela; Ullrich, Tina; Kratzsch, Jürgen; Dittrich, K.; Herberth, Gunda; Adams, Volker; Kieß, Wieland; Erbs, Sandra; Körner, Antje

doi:10.1210/jc.2011-2937

Cited by 153 publications

(152 citation statements)

References 34 publications

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“…Interestingly, high chemerin levels were recently associated with endothelial activation in obese children [42]. The relatively subtle differences observed by us in the levels of these circulating proteins between lean and obese individuals are in agreement with other studies [39,42]. Local concentrations (i.e.…”

Section: Discussionsupporting

confidence: 92%

“…All of these mediators act at the crossroads of metabolism and inflammation, and have been associated with decreased insulin sensitivity in mouse models, obese adults and obese children [38][39][40][41]. Interestingly, high chemerin levels were recently associated with endothelial activation in obese children [42]. The relatively subtle differences observed by us in the levels of these circulating proteins between lean and obese individuals are in agreement with other studies [39,42].…”

Section: Discussionsupporting

confidence: 91%

“…Second, the relatively small obese and lean control groups, and the wide agerange of our participants could have masked differences between lean and obese children. Thus while we report a significant correlation between chemerin and BMI-SD, an even stronger correlation was recently observed in a larger cohort with older children [42]. At the same time, subtle differences in inflammatory mediators may also have been missed due to the relatively small groups with a wide age-range.…”

Section: Discussionsupporting

confidence: 39%

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Systemic inflammation in childhood obesity: circulating inflammatory mediators and activated CD14++ monocytes

et al. 2012

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Aims/hypothesis In adults, circulating inflammatory mediators and activated CD14 ++ monocytes link obesity to its metabolic and cardiovascular complications. However, it is largely unknown whether these inflammatory changes already occur in childhood obesity. To survey inflammatory changes during the early stages of obesity, we performed a comprehensive analysis of circulating inflammatory mediators, monocyte populations and their function in childhood obesity. Methods In lean and obese children aged 6 to 16 years (n0 96), 35 circulating inflammatory mediators including adipokines were measured. Hierarchical cluster analysis of the inflammatory mediator profiles was performed to investigate associations between inflammatory mediator clusters and clinical variables. Whole-blood monocyte phenotyping and functional testing with the toll-like receptor 4 ligand, lipopolysaccharide, were also executed. Results First, next to leptin, the circulating mediators chemerin, tissue inhibitor of metalloproteinase 1, EGF and TNF receptor 2 were identified as novel inflammatory mediators that are increased in childhood obesity. Second, cluster analysis of the circulating mediators distinguished two obesity clusters, two leanness clusters and one mixed cluster. All clusters showed distinct inflammatory mediator profiles, together with differences in insulin sensitivity and other clinical variables. Third, childhood obesity was associated with increased CD14 ++ monocyte numbers and an activated phenotype of the CD14 ++ monocyte subsets. Conclusions/interpretation Inflammatory mediator clusters were associated with insulin resistance in obese and lean ++ monocyte subsets, which is associated with increased development of atherosclerosis in obese adults, was also readily detected in obese children. Our results indicate that inflammatory mechanisms linking obesity to its metabolic and cardiovascular complications are already activated in childhood obesity.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 39%

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Systemic inflammation in childhood obesity: circulating inflammatory mediators and activated CD14++ monocytes

et al. 2012

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“…Chemerin has been also shown to be an independent predictor for the number of white blood cells (Landgraf et al 2012). We clearly showed increased circulating and gene expression levels of this protein in PBMC in both groups of obese patients.…”

Section: Discussionsupporting

confidence: 53%

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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“…Chemerin, a novel adipokine at the crossroad between inflammation and obesity, may possibly influence the vascular endothelium as well. In obese children, increased circulating levels of chemerin have been observed (44), closely correlating with the degree of endothelial dysfunction. Also, addition of chemerin to cultured endothelial cells upregulated the expression of adhesion molecules for white blood cells.…”

Section: Review Bruyndonckx Et Almentioning

confidence: 99%

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

et al. 2016

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Chemerin as a Mediator between Obesity and Vascular Inflammation in Children

Abstract: Our results suggest an association of chemerin with obesity and inflammatory and endothelial activation markers and support a role for chemerin as a molecular link between increasing fat mass and an early atherogenic risk profile in obese children.

Cited by 153 publications

References 34 publications

Systemic inflammation in childhood obesity: circulating inflammatory mediators and activated CD14++ monocytes

Systemic inflammation in childhood obesity: circulating inflammatory mediators and activated CD14++ monocytes

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

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

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