Role of Fibre in Nutritional Management of Pancreatic Diseases

The role of fibre intake in the management of patients with pancreatic disease is still controversial. In acute pancreatitis, a prebiotic enriched diet is associated with low rates of pancreatic necrosis infection, hospital stay, systemic inflammatory response syndrome and multiorgan failure. This protective effect seems to be connected with the ability of fibre to stabilise the disturbed intestinal barrier homeostasis and to reduce the infection rate. On the other hand, in patients with exocrine pancreatic insufficiency, a high content fibre diet is associated with an increased wet fecal weight and fecal fat excretion because of the fibre inhibition of pancreatic enzymes. The mechanism by which dietary fibre reduces the pancreatic enzyme activity is still not clear. It seems likely that pancreatic enzymes are absorbed on the fibre surface or entrapped in pectin, a gel-like substance, and are likely inactivated by anti-nutrient compounds present in some foods. The aim of the present review is to highlight the current knowledge on the role of fibre in the nutritional management of patients with pancreatic disorders

Serotonin and melatonin immunoreactivity in human gastrointestinal tract

Serotonin (5HT) is produced by gut enterochromaffin (EC) cells and is involved in the pathogenesis of neuromotor disorders that characterize functional and inflammatory gastrointestinal diseases. Melatonin is a synthetic product of both the vertebrate pineal gland and the EC cells of gastrointestinal tract (GIT). Both melatonin and serotonin share the same biosynthetic pathway from tryptophan, but their effects are almost antagonistic. Melatonin in the GIT serves as a natural inhibitor of serotonin action on peristalsis, serotonin-induced spastic contractions of rat ileum being reverted by melatonin. Besides, melatonin is a powerful antioxidant that modulates immunological GIT system. Studies on the distribution of EC cells in normal human GIT date back to the nineteen-seventies and, although melatonin has been found in mammal and human gastrointestinal tract, to date there are not clear morphological data on the distribution of melatonin immunoreactivity in normal human gastrointestinal mucosa and on its relationship with the serotoninergic system. Our aim is to produce an immunohistochemical semiquantitative analysis of melatonin and serotonin in normal human mucosal biopsies from patients submitted to a gastroduodenoscopy or colonoscopy for screening or routinely control. Both serotonin and melatonin immunoreactivities were found throughout gastrointestinal mucosa with different pattern of distribution. EC cells storing 5HT (expressed as percentage of mucosal lining cells) were present from gastric antrum to the rectum, the highest concentration being found in the stomach (7.3±3.37%). After a relative drop of expression in the duodenum (3.83±1.97%), EC cells presence remained stable in the ileum (4.03± 0.91), decreased in the colon (2.57± 1.4) and increased again in the rectum (3.8±1.8). Melatonin immunoreactivity in turn was never clearly evidenced in 5HT immunoreactive EC cells but lined the surface of the mucosa and lumen of intestinal glands. It then appears that, differently from 5HT, melatonin is not stored, but immediately released upon the biosynthesis, into the extracellular fluid and circulation. Our data on 5HT and melatonin distribution in human GIT normal mucosa is essential understand their potential role in inflammatory gastrointestinal diseases