Pancreatic Polypeptide Family: Pancreatic Polypeptide, Neuropeptide Y, and Peptide YY

Taylor, Ian L.

doi:10.1002/cphy.cp060221

Cited by 28 publications

(37 citation statements)

References 445 publications

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“…The PP release in response to food is under vagal cholinergic control (42)(43)(44)(45). PP is known to slow down gastric emptying (46) and to suppress food consumption (45)(46)(47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

Proghrelin peptides: Desacyl ghrelin is a powerful inhibitor of acylated ghrelin, likely to impair physiological effects of acyl ghrelin but not of obestatin

Kumar

Salehi

Rehfeld

et al. 2010

Regulatory Peptides

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Background. Proghrelin, produced by the ghrelin (A-like) cells of the gastric mucosa, gives rise to cleavage products, including desacyl ghrelin, acyl ghrelin and obestatin. The products are thought to be secreted concomitantly. In an earlier study we found acyl ghrelin and obestatin, but not desacyl ghrelin, to suppress the release of hormones from isolated islets of mouse and rat pancreas.Results. Using isolated mouse pancreatic islets to study the suppression of the spontaneous secretion of pancreatic polypeptide (PP) by acyl ghrelin and obestatin, we determined the EC 50 values for the two peptides. For acyl ghrelin it was 2 x 10 -13 M (ranging from 1.7 to 2.8 x 10 -13 M), for obestatin it was 10 -13 M (ranging from 0.3 to 1.1 x 10 -13 M). The Hill coefficient (i.e. the midpoint slope) for the acyl ghrelin dose-response curve was 0.30 (ranging from 0.21 to 0.35); the corresponding value for obestatin was 0.35 (ranging from 0.21 to 0.35). The PP-releasing effect of acyl ghrelin, but not that of obestatin, was counteracted by desacyl ghrelin. The acyl ghrelin dose-response curve was shifted to the right in a parallel manner by increasing concentrations of desacyl ghrelin. A Schild plot was constructed with a slope of 0.78, giving an apparent pA 2 value of 14.Conclusions. The results favour the view that acyl ghrelin and obestatin suppress spontaneous PP secretion at physiologically relevant concentrations and that they act on separate receptors. However, we conclude also that desacyl ghrelin acts as a competitive, surmountable (and quite potent) inhibitor of acyl ghrelin. In view of the allegedly high circulating concentrations of desacyl ghrelin it is to be expected that the effect of acyl ghrelin -but not that of obestatin -will be impaired, in fact probably severely blunted by desacyl ghrelin, thereby compromising the functional significance of circulating acyl ghrelin. In addition, we suggest that isolated pancreatic islets are well suited for studies of receptors to acyl ghrelin and obestatin, and that suppression of PP secretion represents a convenient way to measure the effect of both these peptides.

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Section: Discussionmentioning

confidence: 99%

Proghrelin peptides: Desacyl ghrelin is a powerful inhibitor of acylated ghrelin, likely to impair physiological effects of acyl ghrelin but not of obestatin

Kumar

Salehi

Rehfeld

et al. 2010

Regulatory Peptides

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“…In that study [10] motilin, neurotensin and human pancreatic polypeptide were the most common other ectopically released pep tides. and each has been shown to have effects at high con centrations on esophageal motor and/or LES function [43][44][45], It is unclear whether this hypergastrinemia, another ectopically released hormone or some other effect of the disease per se could be contributing to this high prevalence of esophageal disease in these patients [17,18]. Gastrin infusions can affect LES pressure and gas trointestinal smooth muscle contractility [8,11,12], and it was originally proposed that serum gastrin levels could affect physiologically LES function in normals [8,9,[13][14][15][16]46], Whereas it is generally accepted now that serum gastrin is not a physiological regulation of LES function in normals [17,18], it remains possible in patients with ZES that their marked hypergastrinemia could affect esopha geal function, either above or in combination with one of the other ectopically released gastrointestinal peptides.…”

Section: Discussionmentioning

confidence: 99%

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

et al. 1995

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Manifestations of esophageal disease are present in up to 60% of patients with Zollinger-Ellison syndrome (ZES), although esophageal function has been studied in only a few patients and the prevalence of Barrett’s mucosa is unknown in these patients. It is unclear whether the high prevalence of esophageal disease is related to gastric acid hypersecretion alone or to abnormalities of esophageal motility or lower esophageal sphincter (LES) function in addition. To address these issues in the present study esophageal function was evaluated prospectively in 92 consecutive patients with ZES (66 with active disease, 26 disease-free after curative resection) seen during a 1-year period after controlling acid hypersecretion. In the patients with active disease the mean basal acid output (BAO) was 33 ± 3.0 mEq/h, the maximal acid output (MAO) was 56 ± 4.0 mEq/h, fasting serum gastrin was 8,736 ± 4,813 pg/ml and duration of disease prior to study was 12.5 ± 2.0 years. At the time of manometry, gastric acid secretion was controlled in all patients and no patient had evidence of gastroesophageal reflux disease at upper gastrointestinal endoscopy. Esophageal manometry revealed normal motility in 85% of patients. Eleven percent had low LES pressures, and only 1 % of patients had an elevated LES pressure. The frequency of Barrett’s mucosa (3%) was similar to that found in the general population but much less than that reported in patients with idiopathic GERD. No correlation was noted between LES pressures or manometric abnormalities and the fasting serum gastrin, BAO, MAO or the presence or absence of multiple endocrine neoplasia type I or previous vagotomy. Esophageal manometric results and LES pressure were similar in disease-free patients and those with active ZES. In conclusion, these results suggest that hypergastrinemia or other disease-specific abnormalities are not contributing to the high incidence of esophageal disease in patients with ZES because esophageal function in patients with ZES is similar to normals. Specifically, motility disorders in patients with ZES occur in similar frequency to normals, and LES pressure is normal in most patients. Despite the high levels of acid secretion and prominence of symptoms, the occurrence of Barrett’s mucosa was uncommon (3%) raising the possibility of additional protective mechanisms in patients with ZES.

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“…It was initially isolated from porcine jejunal mucosa (Tatemoto 1982) and is a straight-chain peptide containing 36 amino acid residues and exhibits a high degree of homology with two other brain-gut peptides, pancreatic polypeptide (PP) and neuropeptide Y (NPY) (Taylor 1989;Tatemoto et al 1982). This multigene family is collectively referred to as the "pancreatic-polypeptide family of gut peptides."…”

Section: Peptide Yymentioning

confidence: 99%

Regulation of intestinal glucose absorption: A new issue in animal science

Croom¹,

McBride²,

Bird³

et al. 1998

Can. J. Anim. Sci.

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, I. L. 1998. Regulation of intestinal glucose absorption: A new issue in animal science. Can. J. Anim. Sci. 78: 1-13. Intestinal glucose absorption occurs via Na + -dependent glucose cotransporters (SGLT1) located in the luminal membrane of enterocytes and is driven by an electrochemical gradient maintained by Na + /K + ATPase located on the basolateral membrane. Twenty percent of whole animal energy expenditures can be accounted for by the gastrointestinal tract, most of which is the result of Na + /K + ATPase function. Active intestinal glucose transport is regulated by a number of gastrointestinal peptides such as epidermal growth factor (EGF) and peptide YY (PYY). PYY and EGF can upregulate intestinal glucose absorption by as much as 200-300%. Of special interest is the fact that the energetic costs of intestinal tissue function can vary in relationship to the amount of glucose transported. This value termed "apparent energetic efficiency of glucose uptake" (APEE) may be of value in evaluating the energetic costs of glucose and other nutrients during various physiological and nutritional states. Recent studies suggest that intensive genetic selection for production traits in poultry may result in intestinal absorption being rate-limiting for full phenotypic expression of these traits. Further research is needed to clarify this issue.Key words: Glucose absorption, intestinal, energy metabolism, peptides, genetic selection Croom, W. J., Jr., McBride, B., Bird, A. R., Fan, Y.-K., Odle, J., Froetschel, M. et Taylor, I. L. 1998. Régulation de l'absorption du glucose dans l'intestin : un nouveau sujet de recherche zootechnique. Can. J. Anim. Sci. 78: 1-13. L'absorption du glucose dans l'intestin se fait par des transporteurs de type SGLT1 situés dans la membrane luminale des entérocytes et est activitée par un gradiant électrochimique maintenu par la Na + /K + ATPase située sur la membrane basolatérale. Vingt pour cent des dépenses en énergie de l'animal proviennent du tractus gastrointestinal et la quasi-totalité résultent de l'activité de la Na + /K + ATPase. Le transport actif du glucose dans l'intestin est modulé par un certain nombre de peptides gastrointestinaux comme le facteur de croissance épidermique (EGF) et le peptides YY (PYY). Ces deux derniers peuvent activer l'absorption de glucose dans l'intestin jusqu'à concurrence de 200 à 300 %. Particulièrement intéressant est le fait que les coûts énergétiques de l'activité des tissus intestinaux peuvent varier selon la quantité de glucose transportée. Cette valeur désignée par le terme "efficience énergétique apparente de l'absorption du glucose (APEE)" peut être utile pour évaluer les coûts énergétiques du glucose et d'autres nutriments durant divers états physiologiques et nutritionnels de l'animale. Les recherches récentes indiquent qu'une sélection génétique intensive axée sur les caractères de production en aviculture peut faire que l'absorption intestinale devienne un facteur limitant pour la pleine expression phénotypique de ces caractères. Cette que...

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Pancreatic Polypeptide Family: Pancreatic Polypeptide, Neuropeptide Y, and Peptide YY

Cited by 28 publications

References 445 publications

Proghrelin peptides: Desacyl ghrelin is a powerful inhibitor of acylated ghrelin, likely to impair physiological effects of acyl ghrelin but not of obestatin

Proghrelin peptides: Desacyl ghrelin is a powerful inhibitor of acylated ghrelin, likely to impair physiological effects of acyl ghrelin but not of obestatin

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

Regulation of intestinal glucose absorption: A new issue in animal science

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