Abstract
The present studies were directed to determine whether peptide histidine isoleucine (PHI) affects expression of the gastrin and somatostatin genes and whether such effects may be functionally linked. In separate experiments, the effects of PHI on medium gastrin and somatostatin concentrations, the incorporation of 35S-labelled amino acids into newly synthesized gastrin and somatostatin, and steady state gastrin and somatostatin mRNA were determined. PHI inhibited basal expression of the gastrin gene at all levels examined, while no significant effect on basal somatostatin gene expression could be detected. PHI also decreased carbachol-stimulated antral gastrin release and simultaneously increased somatostatin release. However, in contrast to its structural analogues, secretin and gastric inhibitory peptide, the immunoneutralization of endogenous somatostatin by the administration of specific antibodies did not affect significantly the capacity of PHI to inhibit gastrin release into the culture medium stimulated by carbachol. The results of these studies indicate that PHI exerts a physiological inhibitory effect on antral gastrin cells and that this inhibition may occur at several steps along the biosynthetic pathway. In addition, unlike its structural analogues, PHI inhibition of carbachol-stimulated gastrin release is not functionally linked to its stimulatory effects on somatostatin release.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 89-97 |
| Number of pages | 9 |
| Journal | Molecular and Cellular Endocrinology |
| Volume | 84 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Mar 1992 |
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Keywords
- Gene expression
- Messenger RNA
- Peptide biosynthesis
- Tissue culture
- Vasoactive intestinal peptide
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Endocrinology
Cite this
The effects of peptide histidine isoleucine on antral gastrin and somatostatin. / Wolfe, M. Michael; Chang, Rin; Mailliard, Mark E.; Karnik, Pratima S.
In: Molecular and Cellular Endocrinology, Vol. 84, No. 1-2, 03.1992, p. 89-97.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The effects of peptide histidine isoleucine on antral gastrin and somatostatin
AU - Wolfe, M. Michael
AU - Chang, Rin
AU - Mailliard, Mark E.
AU - Karnik, Pratima S.
PY - 1992/3
Y1 - 1992/3
N2 - The present studies were directed to determine whether peptide histidine isoleucine (PHI) affects expression of the gastrin and somatostatin genes and whether such effects may be functionally linked. In separate experiments, the effects of PHI on medium gastrin and somatostatin concentrations, the incorporation of 35S-labelled amino acids into newly synthesized gastrin and somatostatin, and steady state gastrin and somatostatin mRNA were determined. PHI inhibited basal expression of the gastrin gene at all levels examined, while no significant effect on basal somatostatin gene expression could be detected. PHI also decreased carbachol-stimulated antral gastrin release and simultaneously increased somatostatin release. However, in contrast to its structural analogues, secretin and gastric inhibitory peptide, the immunoneutralization of endogenous somatostatin by the administration of specific antibodies did not affect significantly the capacity of PHI to inhibit gastrin release into the culture medium stimulated by carbachol. The results of these studies indicate that PHI exerts a physiological inhibitory effect on antral gastrin cells and that this inhibition may occur at several steps along the biosynthetic pathway. In addition, unlike its structural analogues, PHI inhibition of carbachol-stimulated gastrin release is not functionally linked to its stimulatory effects on somatostatin release.
AB - The present studies were directed to determine whether peptide histidine isoleucine (PHI) affects expression of the gastrin and somatostatin genes and whether such effects may be functionally linked. In separate experiments, the effects of PHI on medium gastrin and somatostatin concentrations, the incorporation of 35S-labelled amino acids into newly synthesized gastrin and somatostatin, and steady state gastrin and somatostatin mRNA were determined. PHI inhibited basal expression of the gastrin gene at all levels examined, while no significant effect on basal somatostatin gene expression could be detected. PHI also decreased carbachol-stimulated antral gastrin release and simultaneously increased somatostatin release. However, in contrast to its structural analogues, secretin and gastric inhibitory peptide, the immunoneutralization of endogenous somatostatin by the administration of specific antibodies did not affect significantly the capacity of PHI to inhibit gastrin release into the culture medium stimulated by carbachol. The results of these studies indicate that PHI exerts a physiological inhibitory effect on antral gastrin cells and that this inhibition may occur at several steps along the biosynthetic pathway. In addition, unlike its structural analogues, PHI inhibition of carbachol-stimulated gastrin release is not functionally linked to its stimulatory effects on somatostatin release.
KW - Gene expression
KW - Messenger RNA
KW - Peptide biosynthesis
KW - Tissue culture
KW - Vasoactive intestinal peptide
UR - http://www.scopus.com/inward/record.url?scp=0026601057&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026601057&partnerID=8YFLogxK
U2 - 10.1016/0303-7207(92)90075-H
DO - 10.1016/0303-7207(92)90075-H
M3 - Article
C2 - 1353464
AN - SCOPUS:0026601057
VL - 84
SP - 89
EP - 97
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
SN - 0303-7207
IS - 1-2
ER -