During the progression from the lean to the obese state, adipose tissue undergoes hyperplasia as well as hypertrophy in an attempt to cope with the increased demand for triglyceride storage. This requires a high degree of plasticity at both the cellular and at the tissue level. Even though adipose tissue as a whole seems to be a relatively static tissue containing many adipocytes that turn over relatively slowly, these cells are embedded in an environment that can rapidly adapt to the needs of expanding and newly differentiating adipocytes. The extracellular matrix of adipose tissue faces unique challenges with respect to adjusting to the need for remodeling and expansion. In parallel, the vasculature has to adapt to altered requirements for nutrient and oxygen exchange. A decrease in the plasticity of these processes leads to metabolic dysfunction. To maintain a healthy, non-inflamed phenotype, complex regulatory mechanisms are in place to ensure adipocytes and stromal vascular cells efficiently crosstalk to allow adipose tissue to expand upon increased demand for storage of triglycerides. These changes are therefore critically dependent on local production of adipokines that include pro-angiogenic and anti-inflammatory moelcules as well as a complex set of extracellular matrix proteins.