In a previous study, mild to moderate exocrine pancreatic insufficiency, as measured by the secretin-pancreozymin test, was found in 23 (43%) of 53 patients with type-1 diabetes mellitus. Of these 53 patients, 20 (7 of whom initially had an abnormal secretin-pancreozymin test) were available for a follow-up examination 11 years later. Of the 7 patients with abnormal exocrine pancreatic function at the first test, 5 remained abnormal and 2 became normal, whereas of the 13 patients with initially normal pancreatic function the test result remained normal in 11 patients and became abnormal in 2.
View Article and Find Full Text PDFThe invited lectures, the symposia and panels and the printed abstracts of the meetings are the basis for analysis of the development of pancreatic research over the 40 years from 1965 to 2005. 245 invited lectures and 59 symposia, panels and round tables presented and discussed the latest state of the art at the meetings of the European Pancreatic Club (EPC). We analyze in detail the contributions to physiology and biochemistry of the pancreas, the neurohormonal control of pancreatic secretion, cell biology, stimulus-secretion coupling, and cell receptors.
View Article and Find Full Text PDFThe European Pancreatic Club (EPC) was founded during a first symposium on December 9 and 10, 1965 in London (President H.T. Howat).
View Article and Find Full Text PDFThe discoverers of secretin already thought of the existence of a chemical excitant for the internal secretion of the pancreas. Numerous experiments have been performed and published between 1906 and 1935 testing the effect of injected or ingested duodenal ("secretin") extracts on fasting or elevated blood glucose levels of normal or diabetic animals and humans with contradictory results. In 1940, after a series of negative dog experiments performed by an opinion leader, the existence of an incretin was considered questionable and further research stopped for more than 20 years.
View Article and Find Full Text PDFGlucagon-like peptide 1 (GLP-1) is a gut (incretin) hormone with multiple actions that could potentially contribute to an antidiabetic effect. This includes: (a) glucose-dependent insulinotropic actions; (b) glucagonostatic actions; (c) a reduction in appetite/promotion of satiety leading to reduced food intake and weight reduction; (d) the deceleration of gastric emptying; and (e) the stimulation of islet growth, differentiation and regeneration. Thus, multiple aspects of the type 2 diabetic phenotype can potentially be improved or even corrected by GLP-1.
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