Obesity stands as a public health issue. Obesity prevalence is increasing throughout every industrialized country. Android obesity is linked with an increased cardiovascular mortality and with type 2 diabetes mellitis, thus calling for an early management of this disease. Several studies showed a significant association between an android fat distribution and an increased cortisol secretion, raising the still debated question of a causal relationship between the development of android obesity and hypercorticism. Moreover, android obese subjects exhibit reduced plasma testosterone and growth hormone levels, meaning complex hormonal abnormalities in these subjects. Current hypotheses suggest that android fat distribution depends on the association of these hormonal abnormalities. Android obese patients have supranormal free fatty acid plasma concentrations. Visceral fat tissue, through its portal drainage, could be an important source for free fatty acids that may exert complex metabolic effects: involvement in hepatic lipogenesis, increase in hepatic neoglucogenic flux, reduction in insulin metabolic clearance and involvement in peripheral insulin resistance through a competition mechanism described by Randle. Technics in vitro (isolated adipocytes) and in vivo in human (labelled fatty acid flux) showed that visceral fatty acid flux was increased in obese patients and subcutaneous adipose tissue, as opposed to common opinion, was also involved in free fatty acid pool in obese patients. Thus, visceral obesity and diabetes could be linked through an enhanced fatty acid availability from adipose tissues (visceral and subcutaneous) in otherwise genetically type 2 diabetes-prone individuals.