Leon Adams and associates1 rightly state that obesity is associated with nonalcoholic fatty liver disease (NAFLD). In particular, visceral adiposity is highly correlated with NAFLD, whereas the correlation with subcutaneous obesity is weaker.2
Intra-abdominal fat delivers fatty acids directly into the portal vein, promoting insulin resistance.2 Patients with truncal obesity have very low levels of adiponectin and high levels of tumour necrosis factor-α (TNF-α).3 Secretion of TNF-α from adipose tissue is strongly associated with obesity-related insulin resistance, which suggests that TNF-α may function in a paracrine fashion in adipose tissue; in contrast, expression of adiponectin from adipose tissue is associated with higher degrees of insulin sensitivity and lower TNF-α expression.4 In addition, TNF-α has been shown to decrease levels of adiponectin.5 Thus, a combination of increased TNF-α and decreased adiponectin leads to severe insulin resistance, which in turn leads to NAFLD. Various treatments for NAFLD (e.g., weight loss or use of drugs such as thiazolidinediones) serve to increase adiponectin levels.5,6
Adams and associates,1 in their discussion of the inflammatory and fibrotic mediators of NAFLD, suggest that adiponectin promotes liver fibrosis in NAFLD, but the evidence indicates that the opposite is true. Some clarification seems warranted.