Chemerin is associated with markers of inflammation and components of the metabolic syndrome but does not predict coronary atherosclerosis.
OBJECTIVE
Chemerin is a recently discovered adipokine that regulates adipocyte differentiation and modulates chemotaxis and activation of dendritic cells and macrophages. Given the convergence of adipocyte and macrophage function, chemerin may provide an interesting link between obesity, inflammation and atherosclerosis in humans. We sought to examine the relationship of i) chemerin and markers of inflammation, ii) chemerin and components of the metabolic syndrome, and iii) chemerin and coronary atherosclerotic plaque burden and morphology.


METHODS
Serum chemerin levels were determined in 303 patients with stable typical or atypical chest pain who underwent dual-source multi-slice CT-angiography to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed, or non-calcified.


RESULTS
Chemerin levels were highly correlated with high sensitivity C-reactive protein (r=0.44, P<0.0001), interleukin-6 (r=0.18, P=0.002), tumor necrosis factor-alpha (r=0.24, P<0.0001), resistin (r=0.28, P<0.0001), and leptin (r=0.36, P<0.0001) concentrations. Furthermore, chemerin was associated with components of the metabolic syndrome including body mass index (r=0.23, P=0.0002), triglycerides (r=0.29, P<0.0001), HDL-cholesterol (r=-0.18, P=0.003), and hypertension (P<0.0001). In bivariate analysis, chemerin levels were weakly correlated with coronary plaque burden (r=0.16, P=0.006) and the number of non-calcified plaques (r=0.14, P=0.02). These associations, however, were lost after adjusting for established cardiovascular risk factors (odds ratio, OR 1.17, 95% confidence interval (CI) 0.97-1.41, P=0.11 for coronary plaque burden; OR 1.06, 95% CI 0.96-1.17, P=0.22 for non-calcified plaques).


CONCLUSIONS
Chemerin is strongly associated with markers of inflammation and components of the metabolic syndrome. However, chemerin does not predict coronary atherosclerosis.
Lehrke
Michael
M
Department of Internal Medicine II, University of Munich, Campus Grosshadern, Marchioninistrasse 15, 81377 Munich, Germany.
Becker
Alexander
A
Greif
Martin
M
Stark
Renee
R
Laubender
Rüdiger P
RP
von Ziegler
Franz
F
Lebherz
Corinna
C
Tittus
Janine
J
Reiser
Maximilian
M
Becker
Christoph
C
Göke
Burkhard
B
Leber
Alexander W
AW
Parhofer
Klaus G
KG
Broedl
Uli C
UC
D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D018925:Chemokines / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000097:blood* / Q000276:immunology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000276:immunology; D007249:Inflammation / Q000097:blood / Q000276:immunology; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000276:immunology; D008875:Middle Aged; D012044:Regression Analysis; D052243:Resistin / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D018925:Chemokines; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D020738:Leptin; C478630:RARRES2 protein, human; D052243:Resistin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D002784:Cholesterol