Systemic chemerin is related to inflammation rather than obesity in type 2 diabetes

Weigert, Johanna; Neumeier, Markus; Wanninger, Josef; Filarsky, Michael; Bauer, Sabrina; Wiest, Reiner; Farkas, S.; Scherer, Marcus N.; Schäffler, Andréas; Aslanidis, Charalampos; Schölmerich, Jürgen; Buechler, Christa

doi:10.1111/j.1365-2265.2009.03664.x

Cited by 251 publications

(228 citation statements)

References 31 publications

(76 reference statements)

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“…Studies in humans have demonstrated a strong correlation between circulating chemerin levels and markers of inflammation and the metabolic syndrome (Lehrke et al 2009, Spiroglou et al 2010, Weigert et al 2010, Dong et al 2011, Gao et al 2011, Ernst et al 2012). Yet, the circulating levels of TNFa and expression of proinflammatory cytokines in adipose tissue were not increased in ChemR23-deficient mice, even after they had been fed a HFD for 20 weeks.…”

Section: Figurementioning

confidence: 99%

ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation

Rouger¹,

Denis²,

Luangsay³

et al. 2013

Journal of Endocrinology

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Chemerin was initially described as a chemoattractant factor for leukocyte populations. More recently, the protein has also been reported to be an adipokine, regulating adipocyte differentiation in vitro via its receptor ChemR23, and to be correlated with BMI and other parameters of the metabolic syndrome in humans. The aim of this study was to investigate the role of the chemerin/ChemR23 axis in the regulation of metabolism in vivo, using a mouse knockout (KO) model for ChemR23 (Cmklr1) in a C57BL/6 genetic background. Body weight and adipose tissue mass did not differ significantly in young animals, but were significantly higher in ChemR23 KO mice aged above 12 months. Glucose tolerance was unaffected. No significant modifications in the levels of blood lipids were observed and no increase in the levels of inflammatory markers was observed in the adipose tissue of KO mice. A high-fat diet did not exacerbate the obese phenotype in ChemR23 KO mice. No obvious defect in adipocyte differentiation was detected, while a marker of lipogenic activity (GPD1 expression) was found to be elevated. In conclusion, the chemerin/ChemR23 system does not appear to play a major role in adipocyte differentiation in vivo, but it may be involved in adipose tissue homeostasis.

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Section: Figurementioning

confidence: 99%

ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation

Rouger¹,

Denis²,

Luangsay³

et al. 2013

Journal of Endocrinology

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“…Chemerin is one of the ligands of CMKLR1 and circulating levels are increased in obesity (Meder et al, 2003;Weigert et al, 2010). Serum chemerin positively correlates with BMI, Homeostasis Model Assessment of Insulin Resistance, triglycerides, systolic blood pressure, leptin, resistin, C-reactive protein, TNF and IL-6 and negatively with HDL cholesterol suggesting a function of chemerin in metabolic disturbances associated with obesity (Bozaoglu et al, 2007;Parlee et al, 2010;Stejskal et al, 2008;Weigert et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Adiponectin upregulates hepatocyte CMKLR1 which is reduced in human fatty liver

Wanninger¹,

Walter²,

Bauer³

et al. 2012

Z Gastroenterol

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Chemokine-like receptor 1 (CMKLR1) ligands chemerin and resolvin E1 are suggested to have a role in non-alcoholic fatty liver disease (NAFLD). Here, expression of CMKLR1 in liver cells and NAFLD was studied. CMKLR1 was detected in primary human hepatocytes (PHH), Kupffer cells, bile-duct cells and hepatic stellate cells. In human and rodent fatty liver and in fibrotic liver of mice fed a methionine-choline deficient diet CMKLR1 was reduced. Hepatocytes are the major cells in the liver and effects of adipokines, cytokines and lipids on CMKLR1 in PHH were analyzed. Increased cellular triglyceride or cholesterol content, lipopolysaccharide, IL-6, TNF and leptin did not influence CMKLR1 levels in PHH whereas profibrotic TGFβ tended to reduce CMKLR1. Adiponectin strongly upregulated CMKLR1 mRNA and protein in PHH and hepatic CMKLR1 when injected into wild type mice. Further, CMKLR1 was suppressed in the liver of adiponectin deficient mice. These data indicate that low CMKLR1 in NAFLD may partly result from reduced adiponectin activity.

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“…The association between chemerin and diastolic dysfunction may be explained by the chronic inflammatory environment of psoriasis. Weigert et al [29] suggested that elevated serum chemerin was strongly related to CRP. Previous reports have shown that CRP decreases the production of nitric oxide and upregulates the expression of angiotensin type-1 receptor, which is associated with endothelial dysfunction [30,31].…”

Section: Discussionmentioning

confidence: 99%