No abstract

In patients with diabetes mellitus and gastroparesis, dysrhythmias of gastric myoelectrical activity, especially tachygastrias, are thought to be involved in the pathogenesis of dyspeptic symptoms. Using surface electrogastrography we studied the prevalence of these abnormalities, and their relationships to dyspeptic symptoms and the extent of cardiac autonomic neuropathy in 30 euglycemic patients with type I diabetes mellitus and 12 controls. Neither in the fasting nor in the postprandial state were differences in mean frequency of gastric electrical control activity and its variability found between patients and controls. In the fasting state, the power content of the 3 cpm component in the power spectrum of the electrogastrogram was even higher in patients than in controls (P = 0.049). In the fasting state, second harmonics of the 3 cpm fundamental gastric signal were seen more often in patients than in controls (P = 0.03). In patients with symptoms during the study, no second harmonics were found after the meal. The postprandial/fasting power ratio was decreased in patients with symptoms during the study as compared to patients without symptoms and controls (P < 0.05). The incidence of dysrhythmias, such as tachygastrias and bradygastrias, was not higher in patients than in controls (17% and 8%, respectively). No correlation was found between electrogastrographic parameters and the severity of autonomic neuropathy or dyspeptic symptoms scored before the study. In conclusion, this study has shown that patients with type I diabetes mellitus and autonomic neuropathy studied under euglycemic conditions do not have grossly disturbed myoelectrical activity, except when symptomatic during the study.

GI blood loss during exercise is of no clinical importance, at least in our study design with a group of well-trained male subjects who consumed a relatively high amount of fluid (up to 2.3 L). Nevertheless, an increased alpha1-antitrypsin and lysozyme concentration may indicate a transient local mucosal damage with an inflammatory response.

In the rat model, hydrophobic bile salts and cholesterol crystals aggravate biliary pancreatitis, whereas phospholipids have a protective effect.

Prolonged exercise results in gastrointestinal symptoms and a significant interruption of postprandial motility. Only the latter phenomenon depends on the mode of exercise and supplementation.