| Summary: | Obesity is considered as top at risk condition in the world and it is mandatory to identify the physiopathological causes involved in adipose tissue enlargement and related metabolic and cardiovascular health disorders. Environmental, behavioural, genetic, epigenetic and multiple biological factors interact to cause obesity. In this context adipose tissue depots have been under focus in the last decades and pivotal concepts have emerged from the studies of their complex biology. While the white adipose tissue (WAT) is the main energy repository in the body (mobilizing fatty acids according to body needs) thanks to white adipocyte properties, WAT is also a multicellular organ communicating with other body organs (brain, muscles, liver, pancreas, heart, vessels, etc…) via complex networks of endocrine signals. The discovery of leptin in 1994 led to recognize WAT as a master organ at the crossroad of a myriad of physiological interactions to control food intake, energy balance, glucose and lipid metabolism, immunity and reproduction. The phenotype, amount and biology of each WAT component are profoundly altered in human obesity. Adipose plasticity also accounts for the extraordinary capacity of adipose precursors to differentiate into functional cardiomyocytes, osteoblasts, haematopoietic and neural cells, a convenient property for regenerative medicine. Finally, while initially thought to exert a negligible role in humans, the discovery of brown adipose tissue in adults stimulates a novel interest for this tissue with high capacity to oxidize fatty acids
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