Hepatic tumor necrosis factor-α, leptin and adiponectin expression in morbid obese patients: Clinicopathological correlations

SummaryBackgroundNonalcoholic 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.MethodsWe enrolled 40 patients undergoing liver biopsy during bariatric surgery. We analyzed hepatic mRNA and immunohistochemistry of TNF-α, leptin, adiponectin and adiponectin receptor.ResultsThirty 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.ConclusionAlthough 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.