Background: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity. We retrospectively studied the clinicopathology and different hepatic adipocytokine expressions between nonalcoholic steatohepatitis (NASH) and non-NASH in morbid obesity. Methods: We enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor. Results: Thirty patients (75%) presented with NASH, including 11 with mild fibrosis and 19 with advanced fibrosis. The HbA1c (P = 0.000), AST (P = 0.000), ALT (P = 0.000), GGT (P = 0.016) and liver fibrosis (P = 0.028) have statistically difference between NASH and non-NASH groups. Steatosis was the only significant factor (r = 0.348, P <0.05) associated with TNF-α mRNA level. Adiponectin mRNA was inversely associated with C-peptide (r = -0.416, P <0.05) and uric acid level (r = -0.426, P <0.05). The best predictors for TNF-α immunostain were hemoglobin (r = 0.432, P <0.01), AST (r = 0.371, P <0.05), lobular inflammation (r = 0.315, P <0.05), portal inflammation (r = 0.331, P <0.05), and NAS (r = 0.365, P <0.05). Leptin immunostain was correlated with C-peptide (r = 0.356, P <0.05) and portal inflammation (r = 0.334, P <0.05). The AdipoRII immunoexpression was negatively correlated with systolic blood pressure (r = -0.481, P <0.01). Multivariate linear regressions of adipocytokine profile related mostly to age, gender, systolic blood pressure, serum uric acid, steatosis, NAS and portal inflammation. Conclusion: Although different adipocytokines may be associated with NAFLD progression in morbid obesity, their major correlations in the pathogenesis of obesity-related NASH are not clear. Additional confirmatory studies are deserved.
- Hepatic adipocytokines
- Morbid obesity
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics