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At least 1,765 records · Page 98Linked to original sources
PubMed1983

[Demonstration of specific receptors for gastric inhibitory peptide (GIP)].

Receptors for the Gastric Inhibitory Polypeptide (GIP) were characterized in particles enriched in plasma membranes obtained from a transplantable hamster insulinoma. Native GIP, at concentrations between 10(-10) and 10(-6) M, inhibited competitively the binding of 125I-GIP to membranes. The binding was highly specific since, among the peptides tested, only the porcine peptide having N-terminal histidine and C-terminal isoleucine amide (PHI), at high concentration (10(-6) M), inhibited by 17% the binding of 125I-GIP. The existence of these receptors suggested that GIP could act directly on beta-cells.

Animals↗
PubMed2006

[Ghrelin - a novel appetite-stimulating hormone which also affects gastrointestinal functions].

Ghrelin, a novel gastrointestinal peptide with 28 amino acids, is secreted from the A-like cells of the gastric fundus. This peptide hormone does not only promote the release of growth hormone, but also stimulates food intake, gastric motility and cardiac output. Increased plasma ghrelin level has been reported in patients with upper gastrointestinal (GI) disease or in their disease animal model, suggesting its important role in the pathogenesis of upper GI disease.

Appetite↗
PubMed1977

Effects of vasoactive intestinal peptide and pancreatic polypeptide on small bowel propulsion in the rat.

Vasoactive intestinal peptide (VIP) and the newly discovered pancreatic polypeptide (PP), both having been proposed as pathogenetic factors in the watery diarrhea syndrome (WDRA), were intravenously infused into rats in order to study the effect on small bowel propulsion. Simultaneously with the infusion of hormone, radioactive test substance was continuously infused into the duodenum of the conscious animal through a permanent catheter. By recording the distribution of radioactivity along the excised gastrointestinal tract, analyses of small bowel propulsion were possible. After infusion of VIP small bowel transit time was significantly prolonged, and the local propagation velocity was retarded both in the proximal and the distal part of the small bowel. PP did not alter small bowel populations. The heavily retarded transport rate after VIP is a propulsive dysfunction and not inconsistent with the clinical sign of diarrhea.

Animals↗
PubMed1964

THE PANCREAS. III.

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Adrenal Cortex Hormones↗
PubMed1997

[Potential role of gut peptides in stress-induced colonic motor disorder].

OBJECTIVE: To explore the potential role of gut peptide in stress-induced colonic motor disorder. METHODS: In 9 conscious Wistar rats pre-equipped with strain-gauge transducers on ascending and descending colon, colonic motility was recorded before, during and after stress. And colonic transit was evaluated by instilling Cr into the cecum through chronically implanted cannula in each group of 16 rats with or without stress, and then calculating the geometric center (GC) of radioactivity. The contents of VIP, SP, NT, SST, MOT and Leu-ENK in plasma, colonic mucosa and muscle layer were assessed in 16 stressed and 16 control rats. Exogenous peptides (VIP, SP, SST, NT) were intravenously administered in 9 rats to determine the colonic motor response. Also, the effects of peptides on colonic circular muscle strips were investigated. RESULTS: Motor activity was increased after stress, whereas colonic transit was delayed. In the stressed rats, plasma levels of VIP and Leu-ENK were higher than those in controls. The content of Leu-ENK in muscle tissue decreased. Both in vivo and in vitro studies showed that SP and NT excited, whereas VIP and SST inhibited colonic motor activity. CONCLUSION: Release of certain peptides is altered by stress. Increased release of ENK and VIP may be involved in stress-induced colonic motor disorder and in the regulation of "stress hormone" release.

Animals↗
PubMed1985

Interaction of gastric inhibitory polypeptide (GIP) with the insulin-secreting pancreatic beta cell line, In lll: characteristics of GIP binding sites.

The interaction of GIP with its receptors in the hamster pancreatic insulin-secreting beta cell line, In lll, has been analyzed. 125I-labelled GIP used as tracer showed the same affinity as native GIP for the GIP binding sites. Binding of the tracer was time, temperature and cell concentration dependent. It was saturable, reversible and highly specific. Under equilibrium conditions, i.e. 2 hours at 13 degrees C, 20% and 25% of the tracer and of GIP binding sites were inactivated, respectively. Native GIP inhibited binding of 125I-labelled GIP in a dose-dependent manner, saturation of the GIP binding sites being obtained at 3. 10(-7) M peptide. Two types of GIP binding sites were found by Scatchard analysis, a small population with a high affinity for GIP (KD = 7 nM) and a large population with a low affinity (KD = 800 nM). The biphasic dissociation process confirmed the GIP binding sites heterogeneity. Apart from GIP, no peptide tested influenced the binding of the 125I-labelled GIP. The present data represents the first analysis of functionally relevant GIP binding sites in a insulin-secreting cell.

Animals↗
PubMed1997

Peptide YY inhibition of rat gastric enterochromaffin-like cell function.

BACKGROUND & AIMS: The cellular target for peptide YY (PYY) inhibition of gastric acid secretion is unknown. The aim of this study was to determine whether PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a selective Y receptor. METHODS: Isolated rat gastric ECL cells were analyzed in short-term culture for histamine release and for changes in intracellular calcium concentration using video imaging. RESULTS: Gastrin-stimulated histamine release was inhibited with a 50% inhibiting concentration of 2.10(-9) mol/L. Inhibition of histamine release and of calcium entry by PYY and [Pro34]PYY and no effect of PYY(3-36) characterizes an inhibitory Y1 receptor subtype. Reverse-transcription polymerase chain reaction of ECL cell RNA showed that the receptor was the nontruncated Y1 isoform. The inhibitory action of PYY and related peptides on gastrin-stimulated histamine release and calcium signaling was eliminated by pretreatment with 200 ng/mL pertussis toxin. Additive but not synergistic inhibitory effects of PYY and somatostatin on gastrin-stimulated histamine release were observed. CONCLUSIONS: Activation of a Y1 inhibitory receptor subtype present on the gastric ECL cell that inhibits gastrin-induced ECL cell histamine release and Ca2+ entry by activation of a Gi or G(o) class of protein may account for inhibition of gastric acid secretion by PYY released from the small intestine.

Animals↗