The influence of the colon on postprandial glucagon-like peptide 1 (7-36) amide concentration in man

Abstract

Glucagon-like peptide (7-36) amide (GLP-1) is an incretin hormone of the enteroinsular axis released rapidly after meals despite the fact that GLP-1 secreting cells (L-cells) occur predominantly in the distal gut. The importance of these colonic L-cells for postprandial GLP-1 was determined in healthy control subjects and in ileostomy patients with minimal small bowel resection (<5 cm). Subjects were fed a high complex carbohydrate test meal (15·3 g starch) followed by two carbohydratefree, high fat test meals (25 g and 48·7 g fat respectively). Circulating levels of glucose, insulin, glucagon, glucose insulinotrophic peptide (GIP) and GLP-1 were measured over a 9-h postprandial period. For both subject groups the complex carbohydrate test meal failed to elicit a rise in either GIP or GLP-1. However, both hormones were elevated after the fat load although the GLP-1 concentration was significantly reduced in the ileostomist group when compared with controls (P=0·02). Associated with this reduction in circulating GLP-1 was an elevation in glucagon concentration (P=0·012) and a secondary rise in the plasma glucose concentration (P=0·006). These results suggest that the loss of colonic endocrine tissue is an important determinant in the postprandial GLP-1 concentration. Ileostomists should not be assumed to have normal enteroinsular function as the colon appears to have an important role in postprandial metabolism.

Prior short-term consumption of resistant starch enhances postprandial insulin sensitivity in healthy subjects

“…This tallies well with both an observed reduction in hepatic glucose production 12 h after insoluble fibre ingestion [25] and the high amounts of liver glycogen found in rats adapted to a high-RS diet [39]. The colon is an important site for luminal and neurally-stimulated GLP-1 release [40]. GLP-1 has been strongly implicated in postprandial oral glucose tolerance, stimulating insulin release and having independent insulinotropic effects [41].…”

Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract

“…Generally, there is little information on GLP-1 release in IBD patients, so far (7,41,49). In particular, to our knowledge, GLP-1 responses to a normal, mixed meal in noncolectomized patients with UC and in patients with CD have not been studied before.…”

“…Third, autonomic neuropathy (10,16,54) and alterations of intramural neurons (9,28,40,45) have been observed in IBD and might disturb gastrointestinal motility. Finally, there is evidence that release of several gastrointestinal neurohormonal mediators that regulate gastric functions may be altered in IBD (1,7,49,58,59); however, these results were conflicting, and roles of key regulators, particularly CCK, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1) (51) have remained unclear. Disturbed release of gastrointestinal hormones from the inflamed mucosa might also contribute to gastric emptying disturbances in diverticulitis, but no systematic studies have been reported.…”

Gustducin couples fatty acid receptors to GLP-1 release in colon

“…In human subjects with ileostomies, the circulating GLP-1 levels after a fat load are significantly reduced compared with healthy control subjects, suggesting that loss of colonic endocrine tissue is an important determinant in regulating postprandial GLP-1 levels (72). In vivo studies of rodents and humans have shown that increased SCFA production after dietary fiber ingestion increases GLP-1 levels (19,70,97).…”