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Hepatic chemerin mRNA expression is reduced in human nonalcoholic steatohepatitis
Author(s) -
Pohl Rebekka,
Haberl Elisabeth M.,
ReinFischboeck Lisa,
Zimny Sebastian,
Neumann Maximilian,
Aslanidis Charalampos,
Schacherer Doris,
Krautbauer Sabrina,
Eisinger Kristina,
Weiss Thomas S.,
Buechler Christa
Publication year - 2017
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12695
Subject(s) - chemerin , medicine , endocrinology , nonalcoholic fatty liver disease , insulin resistance , steatosis , hepcidin , fatty liver , inflammation , diabetes mellitus , adipokine , disease
Background Chemerin is associated with insulin resistance and is expressed in the liver. Nonalcoholic fatty liver disease ( NAFLD ) is related to impaired insulin sensitivity, but studies evaluating hepatic and serum chemerin in NAFLD resulted in discordant data. Materials and methods Chemerin mRNA was determined in the liver tissue obtained from 33 controls and 76 NAFLD patients. Chemerin serum levels were measured in a different cohort of patients with ultrasound‐diagnosed NAFLD and the respective controls. Hepatic stellate cells and hepatocytes were exposed to selected metabolites and nuclear receptor agonists to study the regulation of chemerin. Effect of recombinant chemerin on hepatocyte released proteins was analysed. Results Hepatic chemerin expression was not related to BMI , gender, type 2 diabetes and hypertension. Chemerin mRNA did not correlate with steatosis and was negatively associated with inflammation, fibrosis and nonalcoholic steatohepatitis ( NASH ) score. Patients with NASH had lower chemerin mRNA compared to those with borderline NASH and controls. Factors with a role in NASH mostly did not regulate chemerin in the liver cells. Of note, liver X receptor agonist reduced chemerin protein. Serum chemerin was not changed in NAFLD . Levels positively correlated with age, waist‐to‐hip ratio, systolic blood pressure, serum FGF 21 and lipocalin 2, and negatively with transferrin saturation. Chemerin induced FGF 21 in supernatants of primary human hepatocytes. Hepcidin, a major regulator of iron homoeostasis and lipocalin 2, were not regulated by chemerin. Conclusion Chemerin mRNA is reduced in the liver of NASH patients, and liver X receptor seems to have a role herein.