The effect of GLP-1 and PYY on acid secretion in man

Wettergren, André; Maina, Pierre; Boesby, S; Holst, JJ

doi:10.1016/0167-0115(96)88136-5

Cited by 2 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…(a) Glucagon-like peptide-1 GLP-1 is cleaved from preproglucagon within the intestine, where it is co-localized in the endocrine L-cells of the distal gut with OXM and PYY (Eissele et al 1992;Wettergren et al 1997). It is highly conserved across a number of species, implying an important physiological role.…”

Section: Products Of Preproglucagon Cleavagementioning

confidence: 99%

Gastrointestinal hormones regulating appetite

Chaudhri

Small

Bloom

2006

Phil. Trans. R. Soc. B

291

212

View full text Add to dashboard Cite

The role of gastrointestinal hormones in the regulation of appetite is reviewed. The gastrointestinal tract is the largest endocrine organ in the body. Gut hormones function to optimize the process of digestion and absorption of nutrients by the gut. In this capacity, their local effects on gastrointestinal motility and secretion have been well characterized. By altering the rate at which nutrients are delivered to compartments of the alimentary canal, the control of food intake arguably constitutes another point at which intervention may promote efficient digestion and nutrient uptake. In recent decades, gut hormones have come to occupy a central place in the complex neuroendocrine interactions that underlie the regulation of energy balance. Many gut peptides have been shown to influence energy intake. The most well studied in this regard are cholecystokinin (CCK), pancreatic polypeptide, peptide YY, glucagon-like peptide-1 (GLP-1), oxyntomodulin and ghrelin. With the exception of ghrelin, these hormones act to increase satiety and decrease food intake. The mechanisms by which gut hormones modify feeding are the subject of ongoing investigation. Local effects such as the inhibition of gastric emptying might contribute to the decrease in energy intake. Activation of mechanoreceptors as a result of gastric distension may inhibit further food intake via neural reflex arcs. Circulating gut hormones have also been shown to act directly on neurons in hypothalamic and brainstem centres of appetite control. The median eminence and area postrema are characterized by a deficiency of the blood-brain barrier. Some investigators argue that this renders neighbouring structures, such as the arcuate nucleus of the hypothalamus and the nucleus of the tractus solitarius in the brainstem, susceptible to influence by circulating factors. Extensive reciprocal connections exist between these areas and the hypothalamic paraventricular nucleus and other energy-regulating centres of the central nervous system. In this way, hormonal signals from the gut may be translated into the subjective sensation of satiety. Moreover, the importance of the brain-gut axis in the control of food intake is reflected in the dual role exhibited by many gut peptides as both hormones and neurotransmitters. Peptides such as CCK and GLP-1 are expressed in neurons projecting both into and out of areas of the central nervous system critical to energy balance. The global increase in the incidence of obesity and the associated burden of morbidity has imparted greater urgency to understanding the processes of appetite control. Appetite regulation offers an integrated model of a brain-gut axis comprising both endocrine and neurological systems. As physiological mediators of satiety, gut hormones offer an attractive therapeutic target in the treatment of obesity.

show abstract

Section: Products Of Preproglucagon Cleavagementioning

confidence: 99%

Gastrointestinal hormones regulating appetite

Chaudhri

Small

Bloom

2006

Phil. Trans. R. Soc. B

291

212

View full text Add to dashboard Cite

show abstract

“…Proglucagon peptides were shown to directly or indirectly inhibit gastric acid secretion by various mechanisms for the different species investigated (Beales and Calam, 1996;Gros et al, 1995;Kirkegaard et al, 1982;Wjdemann et al, 1999). Finally, the simultaneous co-release of PYY and proglucagon-derived peptides by L cells (Brubaker, 1991;Plaisancié et al, 1996) may have had a cumulative effect on the inhibition of gastric acid secretion (Anini et al, 1999;Wettergren et al, 1997).…”

Section: Laforenza Et Almentioning

confidence: 99%

PYY-Tag Transgenic Mice Displaying Abnormal (H+-K+)ATPase Activity and Gastric Mucosal Barrier Impairment

Laforenza

Gastaldi

Rindi

et al. 2003

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY:The mechanism by which the gastrointestinal hormones peptide YY and glucagon inhibit gastric acid secretion is largely unknown. PYY-Tag transgenic mice develop endocrine tumors in the colon that are composed mainly of peptide YY/enteroglucagon-producing L type cells. Therefore we studied the functional activity of such tumors and the gastric functions of PYY-Tag mice. Fasting and fed PYY-Tag transgenic mice and CD1 controls were assayed for circulating levels of peptide YY, glucagon, insulin, and gastrin. The gastric pH was determined and gastric samples were examined for (a) histologic appearance; (b) K ϩ -stimulated p-nitrophenylphosphatase activity and [ 14 C]aminopyrine accumulation of apical and tubulovesicle membranes; (c) adherent mucus determination by Alcian blue recovery; and (d) DNA/RNA/protein epithelial content and in vivo incorporation of [ 3 H]thymidine into DNA. Transgenic mice showed high serum levels of peptide YY and glucagon, increased gastric pH, and a high incidence of gastric ulcers after fasting. p-Nitrophenylphosphatase activity, [14 C] aminopyrine accumulation, and proton pump redistribution from cytoplasmic tubulovesicles to apical membranes were significantly lower in the gastric mucosa of transgenic mice compared with the controls. In addition, the adherent mucus was thinner, and [ 3 H]thymidine incorporation into the DNA was decreased. The abnormal and unregulated levels of circulating peptide YY and glucagon led to gastric acid inhibition and an impairment of gastric barrier function as a result of a striking reduction in epithelial proliferation. (Lab Invest 2003, 83:47-54).

show abstract

The effect of GLP-1 and PYY on acid secretion in man

Cited by 2 publications

References 0 publications

Gastrointestinal hormones regulating appetite

Gastrointestinal hormones regulating appetite

PYY-Tag Transgenic Mice Displaying Abnormal (H+-K+)ATPase Activity and Gastric Mucosal Barrier Impairment

Contact Info

Product

Resources

About