Glucagon-Like Peptide-1 7-36 Amide and Peptide YY Have Additive Inhibitory Effect on Gastric Acid Secretion in Man

Wettergren, André; Maina, Pierre; Boesby, S; Holst, Jens J.

doi:10.3109/00365529709025098

Cited by 58 publications

(32 citation statements)

References 23 publications

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“…Interestingly, our previous study showed that peptide YY (PYY), another gut hormone also produced by intestinal L cells in response to nutrient digestion, stimulated intestinal apo A-IV synthesis without a change in apo A-IV mRNA level (27). GLP-1 and PYY share several functions, such as inhibition of gastric acid secretion (46), upper GI motility (2,30), and food intake (6,21). However, they also have some differences.…”

Section: Discussionmentioning

confidence: 96%

GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats

Qin

Shen

Liu

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

135

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Glucagon-like peptide 1 (GLP-1) is a gastrointestinal hormone secreted in response to meal ingestion by enteroendocrine L cells located predominantly in the lower small intestine and large intestine. GLP-1 inhibits the secretion and motility of the upper gut and has been suggested to play a role in the "ileal brake." In this study, we investigated the effect of recombinant GLP-1-(7-36) amide (rGLP-1) on lipid absorption in the small intestine in intestinal lymph duct-cannulated rats. In addition, the effects of rGLP-1 on intestinal production of apolipoprotein (apo) B and apo A-IV, two apolipoproteins closely related to lipid absorption, were evaluated. rGLP-1 was infused through the jugular vein, and lipids were infused simultaneously through a duodenal cannula. Our results showed that infusion of rGLP-1 at 20 pmol.kg(-1).min(-1) caused a dramatic and prompt decrease in lymph flow from 2.22 +/- 0.15 (SE) ml/h at baseline (n = 6) to 1.24 +/- 0.06 ml/h at 2 h (P < 0.001). In contrast, a significant increase in lymph flow was observed in the saline (control) group: 2.19 +/- 0.20 and 3.48 +/- 0.09 ml/h at baseline and at 6 h of lipid infusion, respectively (P < 0.001). rGLP-1 also inhibited intestinal triolein absorption (P < 0.05) and lymphatic apo B and apo A-IV output (P < 0.05) but did not affect cholesterol absorption. In conclusion, rGLP-1 dramatically decreases intestinal lymph flow and reduces triglyceride absorption and apo B and apo A-IV production. These findings suggest a novel role for GLP-1 in lipid absorption.

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Section: Discussionmentioning

confidence: 96%

GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats

Qin

Shen

Liu

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

135

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“…The effect on pancreatic exocrine secretion was first suspected to be secondary to the inhibition of gastric emptying, but in subsequent studies, GLP-1 was demonstrated to also inhibit pancreatic secretion in response to intraduodenal stimulation (84). The inhibitory effect of GLP-1 on acid secretion could be elicited by physiological elevations of the GLP-1 concentrations in plasma and was, remarkably, additive to the inhibitory effects of PYY, which is released from the L-cell in parallel with GLP-1 (324). Together the two peptides almost abolished gastrin-stimulated secretion, indicating that these two peptides are the likely mediators of the "ileal brake effect," i.e., the endocrine inhibition of upper gastrointestinal functions elicited by the presence of unabsorbed nutrients in the ileum (113,163,249).…”

Section: E Effects On the Gastrointestinal Tractmentioning

confidence: 99%

The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,655

2,385

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Glucagon-like peptide 1 (GLP-1) is a 30-amino acid peptide hormone produced in the intestinal epithelial endocrine L-cells by differential processing of proglucagon, the gene which is expressed in these cells. The current knowledge regarding regulation of proglucagon gene expression in the gut and in the brain and mechanisms responsible for the posttranslational processing are reviewed. GLP-1 is released in response to meal intake, and the stimuli and molecular mechanisms involved are discussed. GLP-1 is extremely rapidly metabolized and inactivated by the enzyme dipeptidyl peptidase IV even before the hormone has left the gut, raising the possibility that the actions of GLP-1 are transmitted via sensory neurons in the intestine and the liver expressing the GLP-1 receptor. Because of this, it is important to distinguish between measurements of the intact hormone (responsible for endocrine actions) or the sum of the intact hormone and its metabolites, reflecting the total L-cell secretion and therefore also the possible neural actions. The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions. It also inhibits gastrointestinal motility and secretion and thus acts as an enterogastrone and part of the “ileal brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these actions, GLP-1 or GLP-1 receptor agonists are currently being evaluated for the therapy of type 2 diabetes. Decreased secretion of GLP-1 may contribute to the development of obesity, and exaggerated secretion may be responsible for postprandial reactive hypoglycemia.

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“…In human, GLP-1 and PYY are potent inhibitors on sham feeding-induced gastric acid secretion [88]. The additive type of inhibition by postprandial levels of GLP-1 and PYY was also observed with pentagastrin-stimulated gastric acid secretion in human volunteers [87].…”

Section: Pyy Is a Potent Inhibitor Of Gastric Acid Secretionmentioning

confidence: 95%

Central and peripheral regulation of gastric acid secretion by peptide YY

Yang

2002

Peptides

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Peptide YY (PYY) released postprandially from the ileum and colon displays a potent inhibition of cephalic and gastric phases of gastric acid secretion through both central and peripheral mechanisms. To modulate vagal regulation of gastric functions, circulating PYY enters the brain through the area postrema and the nucleus of the solitary tract, where it exerts a stimulatory action through PYY-preferring Y1-like receptors, and an inhibitory action through Y2 receptors. In the gastric mucosa, PYY binds to Y1 receptors in the enterochromaffin-like cells to inhibit gastrin-stimulated histamine release and calcium signaling via a pertussis toxin-sensitive pathway.

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Glucagon-Like Peptide-1 7-36 Amide and Peptide YY Have Additive Inhibitory Effect on Gastric Acid Secretion in Man

Abstract: The present study suggests that the interaction between GLP-1 and PYY in man is of the additive type. The results indicate that GLP-1 and PYY have an important role in the physiologic control of gastric acid secretion.

Cited by 58 publications

References 23 publications

GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats

GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats

The Physiology of Glucagon-like Peptide 1

Central and peripheral regulation of gastric acid secretion by peptide YY

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