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Increased soluble CD36 is linked to advanced steatosis in nonalcoholic fatty liver disease




Soluble CD36 (sCD36) clusters with insulin resistance, but no evidence exists on its relationship with hepatic fat content. We determined sCD36 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 Kleiner's histological scoring system. Serum sCD36 and hepatic CD36 expression was assessed by immunoassay and immunohistochemistry, respectively.


In NAFLD, serum sCD36 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 sCD36 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 sCD36 values was found in NAFLD depending on the histological grade of steatosis (P < 0·001), but not in CHC (= 0·151). Serum sCD36 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 sCD36 (ρ = 0·499, P < 0·001).


Increased serum sCD36 is an independent factor associated with advanced steatosis in NAFLD.