Significance of serum levels of tumor necrosis factor-alpha and interleukin-6 in patients with nonalcoholic fatty liver disease

Abstract

AIM: To evaluate the significance of serum levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in patients with nonalcoholic fatty liver disease (NAFLD). METHODS: Fifty-seven NAFLD patients, including 21 patients with simple steatosis, 29 patients with nonalcoholic steatohepatitis (NASH) and 7 patients with cirrhosis, and 22 healthy control subjects were included in this study. Serum TNF-α and IL-6 levels were determined by enzyme-linked immunosorbent assay (ELISA). Body weight index, blood pressure, serum glucose, serum insulin and serum lipids were also measured to assess insulin resistance and metabolic syndrome complicated with NAFLD. The differences in serum levels of TNF-α and IL-6 between various groups were compared. The association of serum TNF-α and IL-6 levels with homeostasis model assessment of insulin resistance (HOMA-IR) and the risk of metabolic syndrome was analyzed. RESULTS: The levels of serum TNF-α and IL-6 significantly increased in patients with simple steatosis, NASH and cirrhosis compared with normal subjects (all P＜0.05). The levels of serum TNF-α and IL-6 were significantly higher in NASH patients than in patients with simple steatosis or cirrhosis (both P＜0.05). A significant positive correlation was found between serum TNF-α and IL-6 levels and HOMA-IR (r=608, 0.709, both P=0.000). In NAFLD patients complicated with metabolic syndrome, serum TNF-α and IL-6 levels were significantly elevated compared with NAFLD patients without evidence of metabolic syndrome (P＜0.05). A significant correlation was also observed between serum TNF-α and IL-6 levels and the risk of metabolic syndrome (r=0.409 and 0.552; P=0.002 and 0.000, respectively). CONCLUSION: Increased TNF-α and IL-6 production not only plays an important role in the development and progression of NAFLD but also contributes to the development of metabolic syndrome in NAFLD patients by inducing insulin resistance.