peptide-yy and Celiac-Disease

The changes in PYY in several gastrointestinal disorders and their possible clinical implications are reviewed. The changes in PYY seem to be an adaptive response to alterations in the patho-physiological condition caused by the disease. This becomes evident in gastrointestinal disorders such as diabetes gastroenteropathy, inflammatory bowel diseases, celiac disease, systemic sclerosis and post-intestinal resection state. On the other hand, changes in PYY in chronic idiopathic slow transit constipation appear to be primary and could be one of the etiologic factors of the disease. PYY does not seem to be involved in colorectal carcinoma. Although gastrointestinal dysmotility in neuro-muscular diseases is evident, PYY is not affected. The changes in PYY in gastrointestinal disorders could be beneficial in clinical practice. Thus, in cases where an increase or decrease in PYY is desirable, a diet that increases or decreases PYY synthesis and release can be followed, or a receptor agonist or antagonist can be utilized.

Topics: Anorexia; Celiac Disease; Colorectal Neoplasms; Gastrointestinal Diseases; Humans; Inflammatory Bowel Diseases; Neuromuscular Diseases; Peptide YY

To further establish its role in the ileal brake mechanism, we determined the effect of the distal gut hormone peptide YY (PYY) on gallbladder motility and plasma gut hormones during the cephalic phase of meal stimulation.. Eight healthy volunteers were studied in a randomized crossover design, with or without intravenous infusion of a physiological dose of PYY. On each occasion, subjects underwent modified sham feeding followed by real feeding.. PYY reduced gallbladder emptying in response to modified sham feeding from 23 +/- 5% to 5 +/- 7% (P < 0.01) and integrated plasma pancreatic polypeptide from 2337 +/- 397 pmol/L x 90 min to 903 +/- 232 pmol/L x 90 min (P < 0.01). PYY enhanced plasma cholecystokinin in response to real feeding from 53 +/- 9 pmol/L x 90 min to 82 +/- 17 pmol/L x 90 min (P < 0.05), but did not significantly affect maximum gallbladder emptying and tended to decrease plasma pancreatic polypeptide.. Circulating PYY suppresses the cephalic phase of postprandial gallbladder emptying, but not meal stimulated maximum emptying. The results support the hypothesis that the effect of PYY on gallbladder emptying is mediated by vagal-dependent rather than cholecystokinin-dependent pathways.

Topics: Adult; Celiac Disease; Cholecystokinin; Cross-Over Studies; Fasting; Female; Food; Gallbladder Emptying; Humans; Injections, Intravenous; Male; Middle Aged; Pancreatic Polypeptide; Peptide YY; Vagus Nerve

A 61-year old man with coeliac disease and chronic lack of appetite, malabsorption and weight loss, despite the gluten-free diet, was operated because of a sub-diaphragmatic free air due to a small-bowel pneumatosis cystoides intestinalis (PCI). The jejunum showed granulomatous lesions with a honeycombed appearance of air cysts in the submucosa/subserosa. We found overexpression of peptide YY (PYY) into only the jejunum with PCI, while the expression was very weak or absent in the tissue without cysts. One year after surgery, he had no abdominal pain or PCI recurrence. The above chronic symptoms were plausibly attributable to the PYY.

Topics: Celiac Disease; Humans; Jejunum; Male; Middle Aged; Peptide YY; Pneumatosis Cystoides Intestinalis; Treatment Outcome

Previous research indicated that coeliac disease (CD) is associated with type 1 diabetes mellitus (T1DM). However, the gut-brain axis peptide hormones secretion has not been evaluated so far in patients with CD prior to treatment initiation or under treatment, irrespective of patients having concomitant T1DM or not. The aim of the study was therefore to evaluate these gut hormones at the preprandial levels of patients with CD before and under treatment.. Of forty-seven CD children, 12 untreated (UCD), 22 treated with gluten-free diet (TCD) and 13 treated CD with coexisting T1DM (DCD), and 18 healthy controls (HC) were enrolled. Preprandial glucagon-like-peptide-1 (GLP-1), glucose-dependent-insulinotropic-polypeptide (GIP), active amylin, acylated ghrelin (AG), leptin, pancreatic polypeptide (PP) and peptide-tyrosine-tyrosine (PYY) were determined with hormone-map-array technology.. We found in patients with CD compared with HC that the concentration of (i) GLP-1 was reduced remarkably in all patients with CD (P = 0.008), (ii) GIP was lower in patients with UCD (P = 0.008), (iii) amylin was remarkably reduced (P < 0.01) in all patients with CD, (iv) AG was significantly decreased in patients with DCD (P < 0.01), while (v) leptin, PP and PYY were not significantly different. GIP, GLP-1 and amylin levels correlated positively with insulin concentrations (P < 0.001, P = 0.004 and P < 0.01, respectively) in all patients. Amylin and GIP levels were strongly associated with triglycerides concentrations (P < 0.001, for both peptides) in children with CD.. Our study revealed a different secretion pattern of gut-brain axis hormones in children with CD compared with HC. The alterations in the axis were more pronounced in children with both CD and T1DM.

Topics: Adolescent; Case-Control Studies; Celiac Disease; Child; Child, Preschool; Diabetes Mellitus, Type 1; Diet, Gluten-Free; Female; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Ghrelin; Glucagon-Like Peptide 1; Humans; Incretins; Islet Amyloid Polypeptide; Leptin; Male; Pancreatic Polypeptide; Peptide YY

The distal gut hormone peptide YY (PYY) mediates feedback inhibition of gastric acid secretion, gastrointestinal motility, and pancreatic enzyme output. To investigate the influence of maldigestion on PYY, we determined plasma PYY levels in patients with celiac disease under basal conditions and in response to intraduodenal fat. Basal PYY was increased in untreated celiac patients (N = 13) compared to patients on a gluten free diet (N = 9) [15.6 (11.8-27.0) pM vs 12.2 (10.1-13.1) pM; P < 0.05] and compared to control subjects (N = 15) [9.5 (8.3-10.4) pM; P < 0.001]. Integrated PYY in response to intraduodenally infused predigested fat (1071+/-293 pM 80 min) was significantly (P < 0.05) greater than in response to undigested fat (322+/-223 pM 80 min) in six untreated celiacs. Plasma concentrations of PYY and cholecystokinin were strongly correlated (r = 0.79; P < 0.001). We conclude that basal PYY levels in untreated celiac disease are elevated, that predigestion of fat enhances PYY release in these patients, and that PYY secretion is correlated with CCK release.

Topics: Case-Control Studies; Celiac Disease; Cholecystokinin; Corn Oil; Dietary Fats; Digestion; Female; Humans; Male; Middle Aged; Peptide YY

Peptide YY (PYY) is exclusively localized in endocrine cells in the gut, and these cells are most numerous in the distal small intestine, colon, and rectum. We have earlier shown that PYY coexists with enteroglucagon in the gut endocrine cells. High basal and postprandial plasma enteroglucagon concentrations have earlier been found in patients with untreated coeliac disease. PYY circulates in human plasma and is detectable in most healthy adults. We have therefore studied the basal PYY levels in patients with coeliac disease. Marked elevated basal plasma PYY levels were found in patients with coeliac disease compared with an age- and sex-matched control group. The PYY levels were inversely correlated to the concentration of folate acid in serum. The PYY levels were studied in four patients with newly diagnosed disease and had normalized within 8 months on a gluten-free diet.

Topics: Adolescent; Adult; Aged; Celiac Disease; Female; Folic Acid; Glutens; Humans; Male; Middle Aged; Peptide YY; Peptides

Plasma concentrations of peptide YY (PYY), a newly isolated peptide produced by ileal and colonic endocrine cells, were measured in several groups of patients with digestive disorders after a standardized normal breakfast. Peptide YY levels were found to be grossly elevated in patients with steatorrhea due to small intestinal mucosal atrophy (tropical sprue). Basal levels in these patients were 79 +/- 18 pM, which was nearly 10-fold higher than those seen in healthy controls (8.5 +/- 0.8 pM). Patients with steatorrhea due to chronic destructive pancreatitis also had substantially increased basal PYY levels (47.5 +/- 6.3 pM), and their postprandial response was also greater than that of normal subjects. Moderately elevated plasma PYY concentrations were seen in patients with inflammatory bowel disease and patients recovering from acute infective diarrhea. In contrast, patients with diverticular disease, duodenal ulcer, and functional bowel disease had normal PYY responses. These changes in the secretion of PYY responses. These changes in the secretion, may shed light on the physiologic role of this newly discovered peptide and on intestinal adaptation to common digestive disorders.

Topics: Adult; Aged; Celiac Disease; Chromatography, Gel; Colitis, Ulcerative; Colonic Diseases, Functional; Crohn Disease; Diarrhea; Diverticulitis; Duodenal Ulcer; Female; Food; Gastrointestinal Diseases; Gastrointestinal Hormones; Humans; Intestinal Absorption; Male; Middle Aged; Pancreatitis; Peptide YY; Peptides; Radioimmunoassay