Bariatric surgery ameliorates NAFLD in morbidly obese patients

Aims: In western countries the most common liver disease is Non-alcoholic fatty liver disease (NAFLD). In the present study the effects of weight loss on liver injury, markers of hepatocyte apoptosis and cytokines were analysed 4 weeks and 6 months after bariatric surgery in a cohort of obese NAFLD patients. Methods: Blood and liver tissue were retrieved from 79 morbidly obese patients during the bariatric surgery, at week 4 and 6 months after the procedure. 44 patients (37f/7m, mean age 40.3±8.3 y) underwent Roux-en-Y gastric bypass (RYGB) and 35 patients (24f/11m, mean age 47.2±9.4 y) underwent sleeve gastrectomy (SG), respectively. Liver injury was assessed histopathologically and by determining ALT and AST. Cell death was measured by serum-derived total (M65) and caspase cleaved cytokeratin–18 (M30) and confirmed by TUNEL staining of liver tissue. The stress-induced ligand MIC B, adiponectin, fetuin-A and vitamin D (VD) were quantified in serum by ELISA at all 3 time points. Results: After 4 weeks, BMI decreased significantly in patients receiving RYGB or SG. In parallel a significant decrease in cytokeratin–18 levels was observed (M30: pre 343.4±260.6, post 152.9±94.3 U/l, p<0.001; M65: pre 705.9±566.6, post 318.1±175.7 U/l, p<0.001). In contrast significant increases in MIC B concentrations (pre 1.6±0.2, post 6.0±0.6µg/ml, p<0.02), adiponectin (pre 32.0±19.4, post 69.1±53.0µg/ml, p<0.001) and fetuin-A were detected in the early post-surgery period. Irrespective of the bariatric procedure a reduction of fetuin-A and MIC B to initial levels was observed after 6 months. Preoperatively low serum VD increased significantly in the postoperative period and remained elevated. Conclusion: Our findings suggest that bariatric surgery reduces liver injury and hepatocyte apoptosis in obese patients suffering from NAFLD by improving adipokine signaling and VD status. More detailed analyses of adipose tissue derived factors in bariatric surgery are warranted.