Gastrointestinal motility is closely linked to the rate at which nutri
ents become systemically available. Regulation of gastric emptying rep
resents the most important brake against delivery of nutrients to the
intestine in excess of digestive and absorptive capacity. In man, gast
ric emptying is slowed in proportion to the energy density of the meal
, which will level out the rate of energy delivery to the duodenum. St
udies suggest a more rapid gastric emptying in obesity, although the o
pposite has been reported in some experimental settings, Moreover, gas
tric volume is larger in obese individuals and appropriate satiety sig
nals are not triggered in response to gastric distension, Postprandial
intestinal transit time in obesity is similar to that in normal-weigh
t subjects, however, despite this fact, intestinal absorption of nutri
ents is more efficient in obesity. Several regulatory mechanisms for g
astrointestinal motility, such as the autonomous and enteric nervous s
ystems and gastrointestinal regulatory peptides, are also of importanc
e for feeding behaviour and metabolism. Dysfunction of the autonomous
nervous system has been observed, the sensitivity to cholecystokinin i
s decreased in obesity, and plasma concentrations of somatostatin and
neurotensin are lower than in normal-weight subjects. These changes in
regulatory mechanisms favour rapid gastrointestinal transit of ingest
ed nutrients and promote rapid intestinal absorption in obesity and de
creased satiety in response to ingested food. It is presently not know
n whether the observed changes in gastrointestinal motility in obesity
represent a primary feature linked to the pathogenesis of such diseas
e.