Serum chemerin and vaspin in non-alcoholic fatty liver disease.
OBJECTIVE
Chemerin and vaspin are new adipokines which may modulate inflammatory response and insulin sensitivity in non-alcoholic fatty liver disease (NAFLD). The aims of this study were to assess: (1) circulating levels of chemerin and vaspin and their association with liver histology and markers of liver injury in NAFLD patients; and (2) the relationship between the analyzed adipokines and insulin resistance.


METHODS
A total of 41 NAFLD patients with body mass index (BMI) 30.4 +/- 3.3 kg/m(2) [20 with non-alcoholic steatohepatitis (NASH) and BMI 30.3 +/- 3.3 kg/m(2) and 21 with simple steatosis/uncertain NASH (SS/UN) and BMI 30.5 +/- 3.4 kg/m(2)] and 10 healthy volunteers with BMI 24.0 +/- 2.9 kg/m(2) were included in the study.


RESULTS
Serum chemerin concentration was significantly higher in NAFLD patients compared to healthy volunteers (p = 0.009). Serum chemerin was significantly higher in patients with NASH compared to patients with SS/UN (p = 0.009). The homeostasis model assessment for insulin resistance (HOMA-IR) value was higher in patients with NASH than in patients with SS/UN (p = 0.01). Serum chemerin and HOMA-IR were positively associated with NAFLD activity score (r = 0.40, p = 0.02; and r = 0.43, p = 0.008, respectively). Serum chemerin was associated with hepatocyte ballooning degeneration (r = 0.37; p = 0.03), total cholesterol (r = 0.45; p = 0.008) and diastolic blood pressure (r = 0.41; p = 0.02). HOMA-IR was related to fibrosis stage (r = 0.51; p = 0.001) and inflammatory activity grade in portal tracts (r = 0.40; p = 0.01). Serum vaspin correlated with hepatocyte ballooning degeneration (r = 0.31; p = 0.04), alanine aminotransferase and aspartate aminotransferase (r = 0.33, p = 0.03; and r = 0.32, p = 0.04, respectively) and diastolic blood pressure (r = 0.39, p = 0.01).


CONCLUSIONS
This study shows for the first time that chemerin and vaspin serum concentrations are altered in patients with NAFLD. The analyzed adipokines appear to play a pivotal role in the pathogenesis of NAFLD, not only as regulators of insulin sensitivity, but also as mediators of the inflammatory process.
Kukla
Michal
M
Department of Physiology, Medical University of Silesia, Zabrze, Poland. kuklamich@poczta.onet.pl
Zwirska-Korczala
Krystyna
K
Hartleb
Marek
M
Waluga
Marek
M
Chwist
Alina
A
Kajor
Maciej
M
Ciupinska-Kajor
Monika
M
Berdowska
Agnieszka
A
Wozniak-Grygiel
Elzbieta
E
Buldak
Rafal
R
D054392:Adipokines / Q000097:blood; D000328:Adult; D015415:Biomarkers / Q000097:blood; D018925:Chemokines / Q000097:blood*; D005234:Fatty Liver / Q000097:blood*; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D015843:Serpins / Q000097:blood*
D054392:Adipokines; D015415:Biomarkers; D018925:Chemokines; D036341:Intercellular Signaling Peptides and Proteins; C478630:RARRES2 protein, human; C507339:SERPINA12 protein, human; D015843:Serpins