5 pg/mL; P = 0.153). In CHC patients, 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 of serum sCD36 values was found in NAFLD patients depending on the histological grade of steatosis (P < 0.001) but not in those with CHC (P = 0.151). Serum sCD36 concentrations were independently associated with advanced steatosis in NAFLD patients 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 this website variables (OR, 1.002; 95% CI, 1.000 to 1.003;

P = 0.001). Interestingly, in the overall cohort, a significant correlation was observed between serum sCD36 levels and hepatic CD36 expression (rho = 0.499, P <0.001). In check details conclusion, circulating level of sCD36 correlates with the histological grade of steatosis and is an independent factor associated with advanced steatosis in patients

with NAFLD but not in CHC patients. Performance of serum sCD36 as a direct marker of steatosis, however, must be validated in further clinical studies including distinct cohorts of biopsy-proven NAFLD patients. Disclosures: Javier Crespo – Board Membership: MSD, Roche, Janssen, Gilead Manuel Romero-Gomez – Advisory Committees or Review Panels: Roche Farma, SA., MSD, S. A., Janssen, S. A., Abbott, S. A.; Grant/Research Support: Ferrer, S. A. Javier Garda-Samaniego – Consulting: Boehringer-Ingelheim The following people have nothing to disclose: Carmelo García-Monzón, Oreste Lo Iacono, Miguel Fernandez-Bermejo Background and aims: Adipose 上海皓元 tissue insulin resistance and lipotoxicity are key pathognomonic features in nonalcoholic steatohepatitis (NASH). Liraglutide is a once-daily, long-acting glucagon-like peptide 1(GLP-1) analogue that significantly improves glycaemic control, weight and hepatic steatosis. The aim of this phase II mechanistic study was to determine the effect of Liraglutide on insulin sensitivity (hepatic, muscle, adipose), hepatic lipogenesis and markers of adipose inflammation. Methods: 14 patients with biopsy-proven NASH

were randomly assigned to 1.8mg Liraglutide or placebo (once-daily, SC injections) for 12-weeks as part of the metabolic sub-study of the double-blind, randomised, placebo-controlled LEAN trial (clinicaltrials. gov. NCT01237119). At baseline and 12-weeks, patients underwent paired 2-step hyperinsulinaemic euglycaemic clamps incorporating stable isotopes with concomitant adipose tissue microdialysis. Serum adipocyfokines were quantified with Fluorokine® MAP multiplex kits. In-vitro isotope experiments were performed with Huh-7 and primary human hepatocytes from non-diabetic, male donors with normal BMI. Results: 1.8mg Liraglutide significantly decreased weight, waist circumference, HbA1c, fasting glucose, LDL and liver enzymes versus placebo.