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Obesity, a major social and health problem in many countries, is due to the accumulation of white adipose tissue in subcutaneous and visceral depots. The discovery of adipocytes capacity of synthesis of numerous adipocytokines and growth factors and the cross talk between adipocytes and cells of the adipose stromo-vascular fraction had highlighted the role of adipose tissue dysfunction in obesity. In visceral obesity the unbalanced synthesis of pro-and anti-inflammatory adipocytokines contributes to the development of the metabolic syndrome which cumulates the factors that increase the risk for ischemic heart disease and cerebral stroke. Adipose tissue accumulation is associated with a state of chronic inflammation, and local hypoxia is considered its underlying cause due to the hypertrophic or/and the hyperplasic growth of the fat pad. Adipose tissue hypoxia is one of the first pathophysiological changes and was placed as a missing link between obesity and low-grade inflammation present in the metabolic syndrome. Hypoxia is a major trigger for adipose tissue remodeling including adipocyte death, inflammation, tissue fibrosis, and angiogenesis. Recently, the role of hypoxia in brown adipose tissue dysfunction, a tissue presumed as the biologic counterbalance of the metabolic disturbances in human obesity, is discussed.

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