An implantable gastric stimulator (IGS(R)) has been used for the treatment of obesity with promising results. However, possible mechanisms involved with the treatment of obesity using an IGS are not well understood. According to recent clinical and basic studies, it seems that an IGS reduces appetite and increases satiety, attributed to its inhibitory effects on gastric motility and its direct effects on the central nervous system and hormones related to satiety and/or appetite. It has been indicated that chronic gastric stimulation impairs intrinsic gastric myoelectrical activity in the fed state, induces gastric distention in the fasting state and inhibits postprandial antral contractions. The impairment of gastric myoelectrical activity and contractions is associated with impaired digestion and emptying of the stomach, which may lead to early satiety and reduced food intake. The induction of gastric distention in the fasting state results in activation of stretch receptors, causing satiety. It has also been shown that an IGS may have direct regulatory effects on the central nervous system and certain hormones. Modulation of neuronal activities and release of certain hormones with an IGS may also explain the reduction of appetite and the increase of satiety.