Time-Dependent Changes of Serum Gastrin and Gastrin Receptors in the Rat Oxyntic Mucosa after Proximal Gastric Vagotomy

1997 ◽  
Vol 67 (2) ◽  
pp. 186-192
Author(s):  
Angel J. Reina ◽  
Manuel López-Cantarero ◽  
Andrés Gallardo ◽  
Orlando Fuentes ◽  
Diego Gaitán ◽  
...  
1979 ◽  
Vol 66 (3) ◽  
pp. 149-151 ◽  
Author(s):  
I. A. Donovan ◽  
Caroline Owens ◽  
B. G. Clendinnen ◽  
D. W. Griffin ◽  
L. K. Harding ◽  
...  

1996 ◽  
Vol 270 (3) ◽  
pp. G476-G486 ◽  
Author(s):  
X. Q. Ding ◽  
D. Chen ◽  
E. Rosengren ◽  
L. Persson ◽  
R. Hakanson

We compared the responses of rat stomach ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) to food intake, oral treatment with antisecretagogues, NaHCO3, and hypertonic NaCl, antrectomy, intravenous infusion of gastrin-17, the selective cholecystokinin (CCK)-B/gastrin receptor antagonist L-365,260, and the somatostatin analogue RC-160. The serum gastrin concentration and oxyntic mucosal ODC and HDC activities were higher in freely fed rats than in fasted rats. Food intake in fasted rats raised the serum gastrin concentration and the ODC and HDC activities. Ranitidine, omeprazole, and NaHCO3 raised the serum gastrin concentration and activated ODC and HDC. Hypertonic NaCl raised the ODC activity 200-fold, whereas circulating gastrin and HDC activity were increased only moderately. Infusion of gastrin-17 activated HDC but not ODC. L-365,260 prevented the activation of HDC but not of ODC in response to food intake and treatment with omeprazole, NaHCO3, or hypertonic NaCl. Antrectomy prevented the food- and omeprazole-evoked rise in oxyntic mucosal HDC activity but not the rise in ODC activity. RC-160 suppressed HDC activity after food intake and treatment with omeprazole, NaHCO3, or NaCl. In contrast, RC-160 suppressed omeprazole- and NaHCO3-evoked ODC activation but not that evoked by food intake or NaCl. The results support the view that HDC in the oxyntic mucosa is activated by gastrin and suppressed by somatostatin. The induction of ODC is not mediated by gastrin; ODC activation appears to be related to acid inhibition per se or to mucosal maintenance and repair; somatostatin, or rather the lack of it, might contribute to the induction of ODC after acid blockade. The mechanism behind the activation of rat stomach ODC seems to differ depending on the type of stimulus.


1994 ◽  
Vol 267 (2) ◽  
pp. G254-G258 ◽  
Author(s):  
A. K. Sandvik ◽  
R. Dimaline ◽  
R. Marvik ◽  
E. Brenna ◽  
H. L. Waldum

Gastrin release histamine from the oxyntic mucosa, stimulates the enzymatic activity of histidine decarboxylase (HDC), increases HDC mRNA abundance, and has a trophic effect on the enterochromaffin-like (ECL) cell. In the present study, we examined the effect of exogenous gastrin on HDC activity and mRNA and the time scale of increase and decline of HDC activity and mRNA. Rats received intravenous infusion of gastrin-(1-17) in different doses or periods of time. Oxyntic mucosal HDC activity and mRNA abundance increased significantly with serum gastrin concentrations in the physiological range. The onset of response was rapid and maximal for both parameters after 2 h. Poststimulatory decrease was maximal 2 h after cessation of gastrin infusion. Those observations suggest that HDC enzymatic activity and mRNA abundance are important in meal-to-meal regulation of gastric secretion. Furthermore, HDC enzymatic activity and mRNA abundance varied in parallel, indicating that HDC mRNA abundance is important in the overall regulation of gastric mucosal HDC activity.


1991 ◽  
Vol 69 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Masataka Araki ◽  
Mitsuo Nakamura ◽  
Seiichi Takenoshita ◽  
Hirokazu Shoda ◽  
Yukio Nagamachi ◽  
...  

Since accelerated turnover of histamine in oxyntic mucosa may be an important factor in the pathogenesis of peptic ulcers, the effect of dexamethasone and other glucocorticoids on the activity of gastric histidine decarboxylase (HDC) was studied in the rat. The activity of HDC in rat oxyntic mucosa increased significantly after dexamethasone was injected s.c. to rats at doses larger than 0.4 mg/kg body weight. The maximum response of the HDC activity to dexamethasone (4 mg/kg) was observed 8 h after the treatment. The activity of ornithine decarboxylase (ODC) increased at 4 h, while that of DOPA decarboxylase showed no significant change throughout the 16-h period following a single injection of dexamethasone. The mucosal levels of histamine, putrescine, and spermidine rose significantly after the steroid treatment, while the spermine levels remained nearly constant. There was no sex difference in these responses to dexamethasone. Betamethasone showed nearly the same effects as dexamethasone on the decarboxylase activities and the mucosal levels of diamines. Serum gastrin levels showed no significant change for the first 4 h and then rose significantly 8 and 16 h after dexamethasone treatment. Pentagastrin (0.5 mg/kg) increased the HDC activity, while it showed no significant effect on either the mucosal ODC activity or levels of polyamines and histamine. These data suggest that dexamethasone influences the metabolism of histamine and polyamines in rat oxyntic mucosa both directly and via stimulation of gastrin release.Key words: dexamethasone, betamethasone, oxyntic mucosa, histidine decarboxylase, ornithine decarboxylase, DOPA decarboxylase.


2021 ◽  
Vol 35 (5) ◽  
pp. 2196-2204
Author(s):  
Ahmed Elfadadny ◽  
Ahmed S. Mandour ◽  
Rokaia F. Ragab ◽  
Khalaf F. Alsharif ◽  
Gaber El‐Saber Batiha ◽  
...  

1974 ◽  
Vol 66 (5) ◽  
pp. 944-953 ◽  
Author(s):  
Bernard M. Jaffe ◽  
B. Guy Clendinnen ◽  
Robert J. Clarke ◽  
J. Alexander Williams

1994 ◽  
Vol 266 (3) ◽  
pp. G417-G424 ◽  
Author(s):  
M. G. Martin ◽  
S. V. Wu ◽  
G. Ohning ◽  
H. Wong ◽  
J. H. Walsh

This study demonstrates the effectiveness of parenteral and oral anti-somatostatin monoclonal antibody to stimulate gastrin cell activity in suckling rats. Intraperitoneal anti-somatostatin monoclonal antibody increased serum gastrin concentration (> 2-fold), and orally administered antibodies retained their neutralizing capabilities as demonstrated by a 30% induction of gastrin synthesis. Absorption of luminal monoclonal antibody was time dependent and saturable as demonstrated by measurement of serum murine immunoglobulin G and the subsequent effects on serum gastrin and antral gastrin mRNA concentrations. Enhanced gastrin synthesis after oral administration required whole antibody in that enterally delivered F(ab')2 fragments were not absorbed and did not increase serum gastrin concentrations. In addition, pretreatment with excess Fc fragments decreased monoclonal antibody absorption and eliminated the serum gastrin response to oral monoclonal antibody. These results demonstrate that orally administered murine anti-somatostatin monoclonal antibody was rapidly and efficiently absorbed via an Fc-dependent mechanism and retained immunoneutralizing activity against endogenous somatostatin, neutralizing its inhibition of gastrin cell activity. These results indicate that orally administered monoclonal antibodies could potentially be used to determine the role of other peptides and growth factors as potential physiological regulators during the suckling period of postnatal development.


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