| Abstract: | BACKGROUND: Liver steatosis in chronic hepatitis C virus (HCV) infection is multifactorial. Therefore, there is not necessarily a relation between obesity and liver fat.On the other hand, body fat secretes cytokines, and cytokines and oxidative damage play important roles on progression of liver disease. METHODS: We analyzed the relationships between liver fat (assessed by histomorphometry) and trunk and subcutaneous fat (waist perimeter, triceps skinfold, BMI); the relationships between liver and body fat and cytokines (IL-6, TNF-alpha, IL-8, IFN-gamma, IL-4), adipokines (adiponectin and TIMP-1), and serum malondiladehyde and antioxidants (glutathione peroxidase and superoxide dismutase (SOD) activities); and the relationships of these data with histological changes in 40 HCV-infected non-alcoholic patients. RESULTS: Significant correlations were found between liver fat and waist perimeter and BMI, and between serum TIMP-1 and liver fat. Serum TIMP-1 was significantly related to body fat stores; serum IL-6 and IFN-gamma were related to histological inflammation. Patients with waist perimeter >102 cm (men) or 88 cm (women) showed increased liver fat. In 38.8% of non-obese patients, liver fat accumulation was intense. CONCLUSIONS: There is a relationship between visceral fat, serum TIMP-1 and liver steatosis. However, at least in some patients, factors different from mere adiposity play a role in liver steatosis. |
