The increase in circulating inflammatory factors found in obese subjects and the recent discovery of macrophage infiltration in white adipose tissue (WAT) have opened up new fields of investigation, allowing a reevaluation of the pathophysiology of human obesity. The so-called 'low-grade' inflammatory state, which characterizes this complex disease, is revealed by the moderate, but chronic, systemic rise of a growing panel of molecules with proinflammatory functions. The qualitative and quantitative alterations in the production of these molecules (free fatty acids, cytokines) by the different WAT cell types, particularly in the omental fat depot, are considered new factors with the potential to modify local WAT biology and to contribute, via the portal system, to liver alteration. The aim of this review is to present the most upto-date knowledge regarding the relationships between inflammatory processes in WAT and non-alcoholic liver disease in human obesity.