Obesity is linked to a variety of metabolic disorders, such as insulin resistance and atherosclerosis. The increased incidence of obesity has led to rise in interest in the biology of white adipose tissue (WAT). The tissue is no longer considered as a passive fat storage tissue but is a key endocrine and signaling organ secreting a multiplicity of protein factors called adipokines. In obesity, there is an enhanced secretion of a number of adipokines underpinning the role of inflammation in white adipose tissue towards the development of obesity and associated diseases. There is a substantial evidence, particularly from animal studies, that hypoxia develops in adipose tissue as the tissue mass expands in obesity, and the reduction in PO2 is considered to underlie the inflammatory response. The cells present within the WAT respond to hypoxia, by inhibiting the differentiation of pre-adipocytes to adipocytes and instead being transformed into leptin-secreting cells. The dynamic change found in the adipose tissue can be referred to as “adipose tissue remodeling,” in which stromal cells change dramatically in number and type during the course of obesity. Among stromal cells, infiltration of macrophages in the adipose tissue precedes the development of insulin resistance in animal models, suggesting that they are responsible for obesity-related adipose tissue inflammation. Understanding the molecular mechanism underlying adipose tissue remodeling may lead to the identification of novel, therapeutic strategies to prevent obesity-induced adipose tissue inflammation.