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Glycine-extended gastrin enhances somatostatin release from cultured rabbit fundic D-cells.

Beales IL - F1000Res (2013)

Bottom Line: In this study the effect of G-Gly and gastrin on the release of somatostatin from rabbit fundic D-cells was examined.Treatment of D-cells for 24 hours with gastrin or G-Gly individually, significantly enhanced subsequent basal as well as CCK- and GLP-1-stimulated somatostatin release.Gastrin and G-Gly may be important in the longer term regulation of D-cell function.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Norfolk and Norwich University Hospitals NHS Foundation Trust, Norwich, NR4 7UZ, UK ; Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK ; Royal Postgraduate Medical School, Hammersmith Hospital, London, W12, UK.

ABSTRACT
The role of the peptide hormone gastrin in stimulating gastric acid secretion is well established. Mature amidated gastrin is processed from larger peptide precursor forms. Increasingly these processing intermediates, such as glycine-extended gastrin (G-Gly) and progastrin, have been shown to have biological activities of their own, often separate and complementary to gastrin. Although G-Gly is synthesized and secreted by gastric antral G-cells, the physiological functions of this putative mediator are unclear. Gastrin and cholecystokinin (CCK) stimulate the secretion of somatostatin from gastric D-cells as part of the feedback control of gastric acid. In this study the effect of G-Gly and gastrin on the release of somatostatin from rabbit fundic D-cells was examined. D-cells were obtained by collagenase-EDTA digestion and elutriation and cultured for 48 hours. With a 2 hour exposure to the peptides, gastrin but not G-Gly stimulated somatostatin release. Treatment of D-cells for 24 hours with gastrin or G-Gly individually, significantly enhanced subsequent basal as well as CCK- and GLP-1-stimulated somatostatin release. Twenty four hours exposure to gastrin combined with G-Gly synergistically enhanced basal and agonist-stimulated somatostatin release and cellular somatostatin content. Gastrin and G-Gly may be important in the longer term regulation of D-cell function.

No MeSH data available.


Related in: MedlinePlus

Effects of 24 hour pretreatment with gastrin (10 nM), glycine-extended gastrin (G-Gly) (10 nM) or both peptides on subsequent basal and CCK(10 nM)-stimulated somatostatin release from D-cells.D-cells were cultured for 48 hours and then treated for a further 24 hours with peptides as shown, before stimulation with either CCK or control culture medium for 2 hours. Somatostatin-like immunoreactivity released into the media was quantified by radioimmunoassay. Results expressed and mean ± SEM, compared to untreated control cells, n = 8, * p<0.05 compared to relevant basal control, **p<0.05 compared to gastrin or G-Gly as sole pre-treatment.
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f2: Effects of 24 hour pretreatment with gastrin (10 nM), glycine-extended gastrin (G-Gly) (10 nM) or both peptides on subsequent basal and CCK(10 nM)-stimulated somatostatin release from D-cells.D-cells were cultured for 48 hours and then treated for a further 24 hours with peptides as shown, before stimulation with either CCK or control culture medium for 2 hours. Somatostatin-like immunoreactivity released into the media was quantified by radioimmunoassay. Results expressed and mean ± SEM, compared to untreated control cells, n = 8, * p<0.05 compared to relevant basal control, **p<0.05 compared to gastrin or G-Gly as sole pre-treatment.

Mentions: Twenty four hours pretreatment with gastrin enhanced subsequent basal somatostatin release by 13% and CCK-stimulated release by 10% (both P<0.05). G-Gly enhanced basal somatostatin release by 22% and CCK-stimulated release by 24% (both p<0.05) (Figure 2). The combination of gastrin and G-Gly synergistically increased both basal somatostatin release (35%) and subsequent CCK-stimulated somatostatin release (53%) (p<0.05 compared to the effect of either peptide alone) (Figure 2 andTable 2).


Glycine-extended gastrin enhances somatostatin release from cultured rabbit fundic D-cells.

Beales IL - F1000Res (2013)

Effects of 24 hour pretreatment with gastrin (10 nM), glycine-extended gastrin (G-Gly) (10 nM) or both peptides on subsequent basal and CCK(10 nM)-stimulated somatostatin release from D-cells.D-cells were cultured for 48 hours and then treated for a further 24 hours with peptides as shown, before stimulation with either CCK or control culture medium for 2 hours. Somatostatin-like immunoreactivity released into the media was quantified by radioimmunoassay. Results expressed and mean ± SEM, compared to untreated control cells, n = 8, * p<0.05 compared to relevant basal control, **p<0.05 compared to gastrin or G-Gly as sole pre-treatment.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3814918&req=5

f2: Effects of 24 hour pretreatment with gastrin (10 nM), glycine-extended gastrin (G-Gly) (10 nM) or both peptides on subsequent basal and CCK(10 nM)-stimulated somatostatin release from D-cells.D-cells were cultured for 48 hours and then treated for a further 24 hours with peptides as shown, before stimulation with either CCK or control culture medium for 2 hours. Somatostatin-like immunoreactivity released into the media was quantified by radioimmunoassay. Results expressed and mean ± SEM, compared to untreated control cells, n = 8, * p<0.05 compared to relevant basal control, **p<0.05 compared to gastrin or G-Gly as sole pre-treatment.
Mentions: Twenty four hours pretreatment with gastrin enhanced subsequent basal somatostatin release by 13% and CCK-stimulated release by 10% (both P<0.05). G-Gly enhanced basal somatostatin release by 22% and CCK-stimulated release by 24% (both p<0.05) (Figure 2). The combination of gastrin and G-Gly synergistically increased both basal somatostatin release (35%) and subsequent CCK-stimulated somatostatin release (53%) (p<0.05 compared to the effect of either peptide alone) (Figure 2 andTable 2).

Bottom Line: In this study the effect of G-Gly and gastrin on the release of somatostatin from rabbit fundic D-cells was examined.Treatment of D-cells for 24 hours with gastrin or G-Gly individually, significantly enhanced subsequent basal as well as CCK- and GLP-1-stimulated somatostatin release.Gastrin and G-Gly may be important in the longer term regulation of D-cell function.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Norfolk and Norwich University Hospitals NHS Foundation Trust, Norwich, NR4 7UZ, UK ; Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK ; Royal Postgraduate Medical School, Hammersmith Hospital, London, W12, UK.

ABSTRACT
The role of the peptide hormone gastrin in stimulating gastric acid secretion is well established. Mature amidated gastrin is processed from larger peptide precursor forms. Increasingly these processing intermediates, such as glycine-extended gastrin (G-Gly) and progastrin, have been shown to have biological activities of their own, often separate and complementary to gastrin. Although G-Gly is synthesized and secreted by gastric antral G-cells, the physiological functions of this putative mediator are unclear. Gastrin and cholecystokinin (CCK) stimulate the secretion of somatostatin from gastric D-cells as part of the feedback control of gastric acid. In this study the effect of G-Gly and gastrin on the release of somatostatin from rabbit fundic D-cells was examined. D-cells were obtained by collagenase-EDTA digestion and elutriation and cultured for 48 hours. With a 2 hour exposure to the peptides, gastrin but not G-Gly stimulated somatostatin release. Treatment of D-cells for 24 hours with gastrin or G-Gly individually, significantly enhanced subsequent basal as well as CCK- and GLP-1-stimulated somatostatin release. Twenty four hours exposure to gastrin combined with G-Gly synergistically enhanced basal and agonist-stimulated somatostatin release and cellular somatostatin content. Gastrin and G-Gly may be important in the longer term regulation of D-cell function.

No MeSH data available.


Related in: MedlinePlus