Adipose tissue expansion occurs mainly through two processes; expansion of existing adipocytes and/or recruitment of new adipocytes. Hypertrophic, rather than hyperplastic, obesity has long been known to be related to insulin resistance and other aspects of the Bruceantin metabolic syndrome and to be an independent predictor for future type 2 diabetes. Numerous TBPB studies have demonstrated that adipose tissue dysfunction contributes to unfavorable metabolic changes and type 2 diabetes. Key characteristics of a dysfunctional adipose tissue are, in addition to enlarged adipose cells, impaired adipocyte differentiation, inflammation, remodeling and fibrosis and it has been shown to be related to impaired commitment and differentiation of adipocyte precursor cells. Adipocyte differentiation is a complex process tightly regulated by transcriptional regulators whose induction are necessary for adipogenesis and insulin sensitivity, but also by the Wntsignaling pathway whose inhibition is a prerequisite for preadipocyte differentiation. Inappropriate alteration of these pathways is well known to be associated with obesity-related metabolic complications. It has also long been known that obesity is associated with a lowgrade chronic inflammation residing in the adipose tissue. In 2003 two noteworthy publications demonstrated the involvement of adipose tissue macrophage infiltration in obesity and insulin sensitivity, since then the importance of these findings for the development of insulin resistance and type 2 diabetes has been under investigation. There is also a clear connection between adipocytes and macrophages in terms of adipose tissue expansion-related remodeling and its relation to insulin resistance. The remodeling process its associated with local hypoxia, adipocyte cell death and enhanced chemokine secretion dependent on macrophages to create a permissive environment. Adipocytes, in turn, are responsible for the initiation of the macrophage infiltration. However, the chronic inflammatory and hypoxic milieu also activates tissue fibrosis, which becomes pathogenic when not tightly regulated, resulting in changes of the normal tissue structure and function.