Adipose tissue secretes bioactive peptides, termed "adipokines", which act locally and distally through autocrine, paracrine and endocrine signals. Those signals influences the answers of other tissues and organs including hypothalamus, pancreas, liver, sceletal muscles, endotel an immune system. Increased production of most adipokines impacts on multiple functions such as appetite and energy balance, immunity, insulin sensitivity, angiogenesis, blood pressure, lipid metabolism and haemostasis, all of which are linked with cardiovascular disease. Leptin is a critical mediator of energy balance that relays information regarding the depletion or accumulation of fat stores to the brain. Although many of leptin's effects result from a direct action of leptin on hypothalamic neurons, the functional leptin receptor (long-form or leprb) is also found on many tissues outside the central nervous system (CNS), including immune cells. Obese individuals seem to be resistant to the hypothalamic effects of leptin (maybe because of defective blood-brain barrier transport), the catabolic pathways designed to reduce appetite and increase energy expenditure are not activated and excess body weight is maintained). Adipokines like adiponectin and leptin, at least in physiological concentrations, are insulin sparing as they stimulate beta oxidation of fatty acids in skeletal muscle. The role of resistin is less understood. It is implicated in insulin resistance in rats, but probably not in humans. Adiponectin and resistin are adipocyte-derived polypeptide hormones playing a role in metabolic homeostasis. Their plasma levels are inversely (adiponectin) or directly (resistin) correlated to obesity (and in a patients with type 2 diabetes mellitus) and they have opposite effects on insulin sensitivity. Adipocytes secretes also adipsin, factor B and factor C. In-depth understanding of the pathophysiology and molecular actions of adipokines may, in the coming years, lead to effective therapeutic strategies.