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Increased soluble CD 36 is linked to advanced steatosis in nonalcoholic fatty liver disease
Author(s) -
GarcíaMonzón Carmelo,
Lo Iacono Oreste,
Crespo Javier,
RomeroGómez Manuel,
GarcíaSamaniego Javier,
FernándezBermejo Miguel,
DomínguezDíez Agustín,
Rodríguez de Cía Javier,
Sáez Alicia,
Porrero José Luís,
VargasCastrillón Javier,
ChávezJiménez Enrique,
SotoFernández Susana,
Díaz Ainhoa,
GallegoDurán Rocío,
Madejón Antonio,
MiquilenaColina María Eugenia
Publication year - 2014
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.12192
Subject(s) - steatosis , nonalcoholic fatty liver disease , medicine , gastroenterology , odds ratio , fatty liver , confidence interval , insulin resistance , steatohepatitis , endocrinology , disease , insulin
Background Soluble CD 36 ( sCD 36) clusters with insulin resistance, but no evidence exists on its relationship with hepatic fat content. We determined sCD 36 to assess its link to steatosis in nonalcoholic fatty liver disease ( NAFLD ) and chronic hepatitis C ( CHC ) patients. Materials and methods Two hundred and twenty‐seven NAFLD , eighty‐seven CHC , and eighty‐five patients with histologically normal liver ( NL ) were studied. Steatosis was graded by K leiner's histological scoring system. Serum sCD 36 and hepatic CD 36 expression was assessed by immunoassay and immunohistochemistry, respectively. Results In NAFLD , serum sCD 36 levels were significantly higher in simple steatosis than in NL (361·4 ± 286·4 vs. 173·9 ± 137·4 pg/mL, respectively; P < 0·001), but not in steatohepatitis (229·6 ± 202·5 pg/mL; P = 0·153). In CHC, serum sCD 36 levels were similar regardless of the absence (428·7 ± 260·3 pg/mL) or presence of steatosis (387·2 ± 283·6 pg/mL ; P = 0·173). A progressive increase in serum sCD 36 values was found in NAFLD depending on the histological grade of steatosis ( P < 0·001), but not in CHC ( P = 0·151). Serum sCD 36 concentrations were independently associated with advanced steatosis in NAFLD when adjusted by demographic and anthropometric features [odds ratio (OR), 1·001; 95% confidence interval (CI), 1·000 to 1·002; P = 0·021] and by metabolic variables (OR, 1·002; 95% CI, 1·000 to 1·003; P = 0·001). Interestingly, a significant correlation was observed between hepatic CD36 and serum sCD 36 (ρ = 0·499, P < 0·001). Conclusions Increased serum sCD 36 is an independent factor associated with advanced steatosis in NAFLD .