scholarly journals Effects of Flavanols on Enteroendocrine Secretion

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 844 ◽  
Author(s):  
Carme Grau-Bové ◽  
Carlos González-Quilen ◽  
Ximena Terra ◽  
M. Teresa Blay ◽  
Raul Beltrán-Debón ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Peptide Yy ◽  
Ex Vivo ◽  
Human Colon ◽  
Grape Seed ◽  
Beneficial Effects ◽  
Pure Compounds ◽  
Grape Seed Proanthocyanidin ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Some beneficial effects of grape seed proanthocyanidin extract (GSPE) can be explained by the modulation of enterohormone secretion. As GSPE comprises a combination of different molecules, the pure compounds that cause these effects need to be elucidated. The enterohormones and chemoreceptors present in the gastrointestinal tract differ between species, so if humans are to gain beneficial effects, species closer to humans—and humans themselves—must be used. We demonstrate that 100 mg/L of GSPE stimulates peptide YY (PYY) release, but not glucagon-like peptide 1 (GLP-1) release in the human colon. We used a pig ex vivo system that differentiates between apical and basolateral intestinal sides to analyse how apical stimulation with GSPE and its pure compounds affects the gastrointestinal tract. In pigs, apical GSPE treatment stimulates the basolateral release of PYY in the duodenum and colon and that of GLP-1 in the ascending, but not the descending colon. In the duodenum, luminal stimulation with procyanidin dimer B2 increased PYY secretion, but not CCK secretion, while catechin monomers (catechin/epicatechin) significantly increased CCK release, but not PYY release. The differential effects of GSPE and its pure compounds on enterohormone release at the same intestinal segment suggest that they act through chemosensors located apically and unevenly distributed along the gastrointestinal tract.

Gastrointestinal Satiety Signals III. Glucagon-like peptide 1, oxyntomodulin, peptide YY, and pancreatic polypeptide

2004 ◽  
Vol 286 (5) ◽  
pp. G693-G697 ◽  
Author(s):  
Sarah Stanley ◽  
Katie Wynne ◽  
Steve Bloom
Keyword(s):  
Gastrointestinal Tract ◽  
Animal Models ◽  
Eating Behavior ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Gastrointestinal Function ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Many peptides are synthesized and released from the gastrointestinal tract and pancreas, including pancreatic polypeptide (PP) and the products of the gastrointestinal L cells, glucagon-like peptide 1 (GLP-1), oxyntomodulin, and peptide YY (PYY). Whereas their roles in regulation of gastrointestinal function have been known for some time, it is now evident that they also influence eating behavior. This review considers the anorectic peptides PYY, PP, GLP-1, and oxyntomodulin, which decrease appetite and promote satiety in both animal models and humans.

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

2009 ◽  
Vol 297 (5) ◽  
pp. G861-G868 ◽  
Author(s):  
Jutta Keller ◽  
Christoph Beglinger ◽  
Jens Juul Holst ◽  
Viola Andresen ◽  
Peter Layer
Keyword(s):  
Gastrointestinal Tract ◽  
Gastric Emptying ◽  
Plasma Glucose ◽  
Peptide Yy ◽  
Postprandial Plasma Glucose ◽  
Patient Groups ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Upper Gastrointestinal ◽  
Cck Release

It is unclear why patients with inflammation of the distal bowel complain of symptoms referable to the upper gastrointestinal tract, specifically to gastric emptying (GE) disturbances. Thus we aimed to determine occurrence and putative pathomechanisms of gastric motor disorders in such patients. Thirteen healthy subjects (CON), 13 patients with Crohn's disease (CD), 10 with ulcerative colitis (UC), and 7 with diverticulitis (DIV) underwent a standardized 13C-octanoic acid gastric emptying breath test. Plasma glucose, CCK, peptide YY, and glucagon-like peptide-1 (GLP-1) were measured periodically and correlated with GE parameters. Results were given in means ± SD. Compared with CON, GE half time (T) was prolonged by 50% in CD (115 ± 55 vs. 182 ± 95 min, P = 0.037). Six CD, 2 DIV, and 2 UC patients had pathological T (>200 min). Postprandial plasma glucose was increased in all patients but was highest in DIV and correlated with T ( r = 0.90, P = 0.006). In CD, mean postprandial CCK levels were increased threefold compared with CON (6.5 ± 6.7 vs. 2.1 ± 0.6 pmol/l, P = 0.027) and were correlated with T ( r = 0.60, P = 0.041). Compared with CON, GLP-1 levels were increased in UC (25.1 ± 5.2 vs. 33.5 ± 13.0 pmol/l, P = 0.046) but markedly decreased in DIV (9.6 ± 5.2 pmol/l, P < 0.0001). We concluded that a subset of patients with CD, UC, or DIV has delayed GE. GE disturbances are most pronounced in CD and might partly be caused by excessive CCK release. In DIV there might be a pathophysiological link between decreased GLP-1 release, postprandial hyperglycemia, and delayed GE. These explorative data encourage further studies in larger patient groups.

Steviol Glycoside Rebaudioside A Induces Glucagon-like Peptide-1 and Peptide YY Release in a Porcine ex Vivo Intestinal Model

2014 ◽  
Vol 62 (33) ◽  
pp. 8365-8370 ◽  
Author(s):  
Dina Ripken ◽  
Nikkie van der Wielen ◽  
Heleen M. Wortelboer ◽  
Jocelijn Meijerink ◽  
Renger F. Witkamp ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Ex Vivo ◽  
Rebaudioside A ◽  
Steviol Glycoside ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Minireview: Gut Peptides Regulating Satiety

Endocrinology ◽  
2004 ◽  
Vol 145 (6) ◽  
pp. 2660-2665 ◽  
Author(s):  
Maralyn R. Druce ◽  
Caroline J. Small ◽  
Stephen R. Bloom
Keyword(s):  
Body Weight ◽  
Gastrointestinal Tract ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Premature Death ◽  
Gut Peptides ◽  
The United Kingdom ◽  
Glucagon Like Peptide ◽  
Low Levels ◽  
Glucagon Like Peptide 1

Abstract The gastrointestinal tract and the pancreas release hormones regulating satiety and body weight. Ghrelin stimulates appetite, and glucagon-like peptide-1, oxyntomodulin, peptide YY, cholecystokinin, and pancreatic polypeptide inhibit appetite. These gut hormones act to markedly alter food intake in humans and rodents. Obesity is the current major cause of premature death in the United Kingdom, killing almost 1000 people per week. Worldwide, its prevalence is accelerating. There is currently no effective answer to the pandemic of obesity, but replacement of the low levels of peptide YY observed in the obese may represent an effective antiobesity therapy.

scholarly journals Bile acids drive colonic secretion of glucagon-like-peptide 1 and peptide-YY in rodents

2019 ◽  
Vol 316 (5) ◽  
pp. G574-G584 ◽  
Author(s):  
Charlotte Bayer Christiansen ◽  
Samuel Addison Jack Trammell ◽  
Nicolai Jacob Wewer Albrechtsen ◽  
Kristina Schoonjans ◽  
Reidar Albrechtsen ◽  
...  
Keyword(s):  
Bile Acids ◽  
G Protein ◽  
Peptide Yy ◽  
Whole Body ◽  
Rat Colon ◽  
G Protein Coupled Receptor ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

A large number of glucagon-like-peptide-1 (GLP-1)- and peptide-YY (PYY)-producing L cells are located in the colon, but little is known about their contribution to whole body metabolism. Since bile acids (BAs) increase GLP-1 and PYY release, and since BAs spill over from the ileum to the colon, we decided to investigate the ability of BAs to stimulate colonic GLP-1 and PYY secretion. Using isolated perfused rat/mouse colon as well as stimulation of the rat colon in vivo, we demonstrate that BAs significantly enhance secretion of GLP-1 and PYY from the colon with average increases of 3.5- and 2.9-fold, respectively. Furthermore, we find that responses depend on BA absorption followed by basolateral activation of the BA-receptor Takeda-G protein-coupled-receptor 5. Surprisingly, the apical sodium-dependent BA transporter, which serves to absorb conjugated BAs, was not required for colonic conjugated BA absorption or conjugated BA-induced peptide secretion. In conclusion, we demonstrate that BAs represent a major physiological stimulus for colonic L-cell secretion.NEW & NOTEWORTHY By the use of isolated perfused rodent colon preparations we show that bile acids are potent and direct promoters of colonic glucagon-like-peptide 1 and peptide-YY secretion. The study provides convincing evidence that basolateral Takeda-G protein-coupled-receptor 5 activation is mediating the effects of bile acids in the colon and thus add to the existing literature described for L cells in the ileum.

scholarly journals Exogenous glucagon-like peptide 1 reduces contractions in human colon circular muscle

2014 ◽  
Vol 221 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Antonella Amato ◽  
Sara Baldassano ◽  
Rosa Liotta ◽  
Rosa Serio ◽  
Flavia Mulè
Keyword(s):  
Colonic Motility ◽  
Circular Muscle ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Mechanical Activity ◽  
Organ Bath ◽  
Dependent Manner ◽  
Double Labeling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide 1 (GLP1) is a naturally occurring peptide secreted by intestinal L-cells. Though its primary function is to serve as an incretin, GLP1 reduces gastrointestinal motility. However, only a handful of animal studies have specifically evaluated the influence of GLP1 on colonic motility. Consequently, the aims of this study were to investigate the effects induced by exogenous GLP1, to analyze the mechanism of action, and to verify the presence of GLP1 receptors (GLP1Rs) in human colon circular muscular strips. Organ bath technique, RT-PCR, western blotting, and immunofluorescence were used. In human colon, exogenous GLP1 reduced, in a concentration-dependent manner, the amplitude of the spontaneous contractions without affecting the frequency and the resting basal tone. This inhibitory effect was significantly reduced by exendin (9–39), a GLP1R antagonist, which per se significantly increased the spontaneous mechanical activity. Moreover, it was abolished by tetrodotoxin, a neural blocker, or Nω-nitro-l-arginine – a blocker of neuronal nitric oxide synthase (nNOS). The biomolecular analysis revealed a genic and protein expression of the GLP1R in the human colon. The double-labeling experiments with anti-neurofilament or anti-nNOS showed, for the first time, that immunoreactivity for the GLP1R was expressed in nitrergic neurons of the myenteric plexus. In conclusion, the results of this study suggest that GLP1R is expressed in the human colon and, once activated by exogenous GLP1, mediates an inhibitory effect on large intestine motility through NO neural release.

scholarly journals Ileal short-chain fatty acids inhibit gastric motility by a humoral pathway

2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert
Keyword(s):  
Gastric Motility ◽  
Short Chain Fatty Acid ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Maximal Amplitude ◽  
Inhibiting Factor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The aim of this study was to evaluate the nervous and humoral pathways involved in short-chain fatty acid (SCFA)-induced ileal brake in conscious pigs. The role of extrinsic ileal innervation was evaluated after SCFA infusion in innervated and denervated Babkin's ileal loops, and gastric motility was measured with strain gauges. Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) concentrations were evaluated in both situations. The possible involvement of absorbed SCFA was tested by using intravenous infusion of acetate. Ileal SCFA infusion in the intact terminal ileum decreased the amplitude of distal and terminal antral contractions (33 ± 1.2 vs. 49 ± 1.2% of the maximal amplitude recorded before infusion) and increased their frequency (1.5 ± 0.11 vs. 1.3 ± 0.10/min). Similar effects were observed during SCFA infusion in ileal innervated and denervated loops (amplitude, 35 ± 1.0 and 34 ± 0.8 vs. 47 ± 1.3 and 43 ± 1.2%; frequency, 1.4 ± 0.07 and 1.6 ± 0.06 vs. 1.1 ± 0.14 and 1.0 ± 0.12/min). Intravenous acetate did not modify the amplitude and frequency of antral contractions. PYY but not GLP-1 concentrations were increased during SCFA infusion in innervated and denervated loops. In conclusion, ileal SCFA inhibit distal gastric motility by a humoral pathway involving the release of an inhibiting factor, which is likely PYY.

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