It is quite frequent to recognize celiac patients who show gastrointestinal motor abnormalities in clinical practice. In fact, in 30 to 60% of patients, physical examination and dyspeptic symptoms (epigastric discomfort, early satiety) suggest a gastrointestinal motility disorder. Consistent data are now available on the presence of a disturbed motility of the esophagus, stomach, small intestine, gallbladder, and colon of untreated celiac patients. Gastrointestinal abnormalities differ in different gastrointestinal districts. In fact, esophageal transit, gastric and gallbladder emptying, and orocecal transit time are delayed, while colonic transit is faster. These findings are related to the complex interactions among reduced absorption of food constituent (in particular, fat), neurologic alteration, and hormonal derangement. Motility disorders of the gut are also a predisposing factor in the development of small intestinal bacterial overgrowth and may contribute both to development of symptoms in some untreated celiacs and to the persistence of symptoms after gluten-free diet in some of them. All these alterations fortunately disappear after gluten-free diet, and patients return to well being status. Whatever the initial event in the pathogenesis of the celiac lesions may be, we know for certain at this time that gastrointestinal disturbances play an important role in the genesis of gastrointestinal symptoms in celiac disease and that surveillance for celiac disease in patients complaining of dysmotility-like dyspeptic symptoms should be increased.