Implications of altered gastrointestinal motility in obesity.
The onset of obesity occurs as a result of an imbalance between nutrient consumption/absorption and energy expenditure. Gastrointestinal (GI) motility plays a critical role in the rate of consumption of foods, digestion, and absorption of nutrients. Various segments of the GI tract coordinate in a complex yet precise way, to control the process of food consumption, digestion, and absorption of nutrients. GI motility not only regulates the rates at which nutrients are processed and absorbed in the gut, but also, via mechanical and neurohormonal methods, participates in the control of appetite and satiety. Altered GI motility has frequently been observed in obese patients, the significance of which is incompletely understood. However, these alterations can be considered as potential contributing factors in the development and maintenance of obesity and changed eating behavior. Therapies aimed at regulating or counteracting the observed changes in GI motility are being actively explored and applied clinically in the management of obese patients.
D003106:Colon / Q000503:physiopathology; D004558:Electric Stimulation; D002149:Energy Intake; D005746:Gastric Emptying / Q000502:physiology; D005764:Gastroesophageal Reflux / Q000503:physiopathology; D005769:Gastrointestinal Motility / Q000502:physiology*; D006801:Humans; D007421:Intestine, Small / Q000503:physiopathology; D009765:Obesity / Q000503:physiopathology*; D012528:Satiety Response / Q000502:physiology