White adipose tissue is a major endocrine and secretory organ, white adipocytes releasing a multiplicity of protein hormones and factors - adipokines. Many adipokines are linked to the inflammatory response, and inflammation within the enlarged adipose tissue underlies the development of the disorders linked to obesity. Local hypoxia develops as adipose mass expands, large adipocytes becoming O2-deprived. Candidate gene studies with adipocytes in culture have shown that the expression and secretion of key inflammation-related adipokines, including IL-6, leptin and VEGF, are stimulated by low pO2; the production of adiponectin with its anti-inflammatory action is, however, inhibited. Microarray studies have demonstrated that the expression of >650 genes is up- and >600 down-regulated in response to hypoxia. These include the facilitative glucose transporter GLUT1, expression of which increases, and there is a rise in GLUT1 protein linked to a hypoxia-stimulated increase in glucose uptake. Lactate release is also increased, indicative of a switch to glycolytic metabolism. Synthesis of the monocarboxylate transporter, MCT1, is stimulated by hypoxia, enabling increased lactate removal from hypoxic adipocytes. Recent studies have shown that even small reductions in oxygen tension induce changes in the production of key adipokines, including leptin and VEGF, as well as increases in glucose utilisation. Other cells within adipose tissue also respond to hypoxia, the synthesis of leptin being induced in preadipocytes, for example. Hypoxia has a pervasive effect on adipocyte function and is central to the dysregulation of adipose tissue in obesity that underlies insulin resistance and the metabolic syndrome.