Objective To investigate the association of type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) with adipocytokines. Methods One hundred subjects from our medical examination center were included in the study. The control group comprised 47 subjects(group A) and the NAFLD group comprised 53 subjects (group B). One hundred and forty inpatients with T2DM were divided into two groups according to the abdominal ultrasound. Seventy-nine patients had T2DM(group C) and 61 patients had T2DM and NAFLD (group D). All the participants were subjected to measurement of liver function, lipids, blood glucose, insulin, C reactive protein (CRP), uric acid, adiponecin(APN) and tumor necrosis factor-α (TNF-α). Results The body mass, body mass index (BMI), waist circumference, levels of lipids, insulin, HOMA-IR, transaminase and uric acid in group B were significantly higher than those in group A(P＜0.01). β-cell function was significantly lower in group B than in group A(P＜0.01). The levels of fasting insulin, cholesterol, triglycerides(TG), uric acid, alanine aminotransferase (ALT) and γ-glutamyltransferase (GGT) in group B were significantly higher than those in group C(P＜0.01). The body mass, waist circumference, levels of fasting insulin, TG, HOMA-IR, ALT and GGT in group D were significantly higher than those in group C(P＜0.01). The blood pressure and levels of HOMA-IR in group D were higher than those in group B(P＜0.01). The APN levels in group B, C and D were significantly lower (P＜0.01), and TNF-α levels were significantly higher than those in group A(P＜0.01). The APN levels of group D were lower (P＜0.01), and TNF-α levels were higher than those in group B and C (P＜0.01). The logistic regression analysis showed that TG and TNF-α were independent risk factors for NAFLD. The APN was negatively associated with HOMA-IR, TG, waist circumference, TNF-α. And TNF-α was positively associated with fasting insulin, HOMA-IR, negatively associated with APN. Conclusions The adipocytokines probably play a role in the pathophysiology of T2DM and NAFLD, and the restoration of the adipocytokines has some clinical significance.