Gastrointestinal (GI) motility has a crucial role in the food consumption, digestion and absorption, and also controls the appetite and satiety. In obese patients, various alterations of GI motility have been investigated. The prevalence of GERD and esophageal motor disorders in obese patients are higher than those of general population. Gastric emptying of solid food is generally accelerated and fasting gastric volume especially in distal stomach is larger in obese patients without change in accommodation. Contractile activity of small intestine in fasting period is more prominent, but orocecal transit is delayed. Autonomic dysfunction is frequently demonstrated in obese patients. These findings correspond with increased appetite and delayed satiety in obese patients, but causes or results have not been confirmed. Therapeutic interventions of these altered GI motility have been developed using botulinum toxin, gastric electrical stimulation in obese patients. Novel agents targeted for GI hormone modulation (such as ghrelin and leptin) need to be developed in the near future.
Botulinum Toxins/therapeutic use ; Colon/*physiopathology ; Eating ; Electric Stimulation Therapy ; Esophageal Motility Disorders/etiology/*physiopathology/therapy ; *Gastrointestinal Motility ; Ghrelin/therapeutic use ; Humans ; Intestine, Small/*physiopathology ; Leptin/therapeutic use ; Obesity/*complications ; Satiety Response ; Stomach/innervation/*physiopathology