Gastrin cell proliferation after chronic stimulation: effect of vagal denervation or gastric surgery in the rat.

Alumets, J.; Munshid, H. A. El; Håkanson, R.; Hedenbro, Jan; Liedberg, G; Oscarson, J.; Rehfeld, Jens F.; Sundler, F.; Vallgren, S

doi:10.1113/jphysiol.1980.sp013101

Cited by 59 publications

(22 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During the first days of cortisol infusion, antral gastrin content may even have decreased. Acute stimulation of gastrin release by antral exclusion (Alumets, El Mundshid, Hakanson, Hedenbro, Liedberg, Oscarson, Rehfeld, Sundler & Vallgren, 1980) or the stress of birth leads to a decrease in antral gastrin.…”

Section: Discussionmentioning

confidence: 99%

Secretion of acid, gastrin, and cobalamin‐binding proteins by the fetal pig stomach: developmental regulation by cortisol

Sangild¹,

Hilsted²,

Nexø³

et al. 1994

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYThe role of cortisol in the development of gastric function was investigated in the fetal pig. Pregnant sows (term = 1 14 + 2 days, n = 10) were anaesthetized (pentobarbitone) and osmotic minipumps containing either saline or cortisol inserted subcutaneously into fetuses at 82-84 (n = 11) or 91-96 (n = 14) days gestation. Six days later the infused pigs were removed by Caesarean section and the stomach and its contents collected for analysis. Samples were also obtained from unoperated (control) fetal pigs (n = 51) removed under anaesthesia at intervals from 70 days gestation until term. The concentrations of acid in gastric fluid, gastrin in plasma and antral tissue (bioactive as well as precursor forms), and cobalamin(CBL)-binding proteins in fundic tissue were low in control pigs until 100 days gestation. During the last 2 weeks before term, large increases occurred in gastric fluid acidity (from pH 6-7 to pH 3 at birth), plasma amidated gastrin (from 10 to 90 pM) and CBL-binding protein concentration (from 10 to 80 pmol (g fundus)-1). These changes occurred in parallel with a surge in plasma cortisol (from 20 to 200 ng ml-'). Immature fetuses infused with cortisol had significantly higher gastric acidity, plasma amidated gastrin, and concentration of CBL-binding proteins than the corresponding control fetuses (P < 0 05). Across age and treatment groups, significant correlations were found between log1o plasma cortisol values and the above parameters (r = 0 59-076, P < 001). The results suggest that endogenous cortisol secretion stimulates the secretion of gastric acid, gastrin and CBL-binding proteins in the prenatal period of the pig.

show abstract

Section: Discussionmentioning

confidence: 99%

Secretion of acid, gastrin, and cobalamin‐binding proteins by the fetal pig stomach: developmental regulation by cortisol

Sangild¹,

Hilsted²,

Nexø³

et al. 1994

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…and gastrin (B) mRNA levels in antral mRNA with omeprazole-induced achlorhydria. Antral RNA was isolated from rats 4 and 12 h after an omeprazole injection (100l mol/ kg, i.v., bis die) and 1, 2, 3, and 5 d after omeprazole .l0O-ug, bis die intraperitoneal injection, and compared with * mRNA levels in untreated controls. mRNA levels were quantitated by dot-blot hybridization as described in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Achlorhydria, as is seen in atrophic gastritis, releases antral gastrin cells (G cells) from this inhibition and consequently causes marked hypergastrinemia and G-cell hyperplasia (1)(2)(3). Surgical ablation of gastric acid secretion in rats by fundectomy produces similar changes (4) and has also been shown to stimulate gastrin synthesis (5). Chronic blockade of acid secretion with the H+/K+ ATPase antagonist omeprozole results in hypergastrinemia and, with prolonged treatment, in G-cell hyperplasia (6)(7)(8).…”

mentioning

confidence: 92%

Reciprocal regulation of antral gastrin and somatostatin gene expression by omeprazole-induced achlorhydria.

Brand¹,

Stone²

1988

J. Clin. Invest.

167

View full text Add to dashboard Cite

Gastric acid exerts a feedback inhibition on the secretion of gastrin from antral G cells. This study examines whether gastrin gene expression is also regulated by changes in gastric pH. Achlorhydria was induced in rats by the gastric H+/K+ ATPase inhibitor, omeprazole (100 gmol/kg). This resulted in fourfold increases in both serum gastrin (within 2 h) and gastrin mRNA levels (after 24 h).Antral Substantial evidence supports the hypothesis that gastric acid inhibits gastrin secretion through somatostatin released from antral D cells (9, 10). Somatostatin is a potent inhibitor of gastrin release (11). Antral D cells have characteristic cytoplasmic projections onto G cells (12, 13) that may act as a pathway for paracrine inhibition by somatostatin. Since gastric acid stimulates somatostatin release (14-16), gastrin secretion is thought to be inhibited by somatostatin released locally from these cytoplasmic processes. The inhibition ofgastrin secretion by antral somatostatin thus represents a probable example of paracrine regulation. Measurement ofchanges in somatostatin mRNA levels with changes in gastric pH may be of value in evaluating the D cell's role as a paracrine regulator of antral G cells, since these mRNA levels directly reflect D cell activity.Although somatostatin's inhibitory action on gastrin secretion is well established, it is not known whether somatostatin also inhibits gastrin gene expression. In the pituitary, where somatostatin also mediates a similar feedback cycle involving the inhibition of hormone secretion (17), short term incubation with somatostatin does not inhibit growth hormone gene transcription (18). This suggests a dissociation between somatostatin's ability to inhibit pituitary hormone secretion and its effects on hormone synthesis. Consequently, somatostatin may not necessarily inhibit gastrin gene expression despite its well described effects on gastrin secretion. MethodsOmeprazole treatment. Male Sprague-Dawley rats weighing 180-220 g were fed regular laboratory chow ad lib. Omeprazole dissolved in 100 ,gmol/kg PEG 2000 (concentration 20 mg/ml) was injected intraperitoneally twice daily at 12-h intervals (0.2 ml PEG in 1 ml 0.15% NaHCO3). Control rats received intraperitoneal injections of 0.2 mls PEG alone in 1 ml NaHCO3. After an overnight fast, rats were anesthetized with ether, 1.5 ml of their blood was drawn by cardiac puncture, and then they were killed. The antrum was excised, and a similar weight of corpus from the greater curvature adjacent to the saccuscorpus margin was excised. The duodenum, excluding a 2-mm rim adjacent to the pylorus, was also removed. Tissues were immediately placed in guanidium thiocyanate lysis buffer (18) and homogenized using a polytron (Brinkmann Instruments Co., Westbury, NY).RNA preparation. RNA was prepared by the lithium chloride precipitation method of Cathala et al. (19) and the concentration of RNA was measured spectrophotometrically by the absorbance at 260 A. The efficiency of RNA recovery, determined by adding 3H-labeled SP...

show abstract

“…The results are expressed as #um2 cell area or cytoplasm area. The error of this method has been estimated in several previous publications (Alumets, El Munshid, HAkanson, Liedberg, Oscarson, Rehfeld & Sundler, 1979;Alumets, El Munshid, HAkanson, Hedenbro, Liedberg, Oscarson, Rehfeld, Sundler & Vallgren, 1980). It varies from 1-6 to 3-2 %.…”

Section: Electron Microscopymentioning

confidence: 99%

Gastric acid response to pylorus ligation in rats: is gastrin or histamine involved?

Alumets¹,

Ekelund²,

Håkanson³

et al. 1982

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Pylorus ligation stimulated the acid output in vagally intact rats. The serum gastrin concentration and the gastric mucosal histamine content were not affected. The gastric histidine decarboxylase activity was initially slightly elevated and then greatly reduced (12-20 hr after ligation).2. Pylorus ligation stimulated the acid output in chronically, but not in acutely, vagotomized rats. Chronic vagotomy raises the serum gastrin concentration, the gastric histamine content and histidine decarboxylase activity. The serum gastrin concentration was further raised by pylorus ligation. The histamine content was initially lowered but returned to preligation values after 20 hr. The histidine decarboxylase activity first decreased, but increased to very high levels 5-6 hr after ligation. Twelve hours after ligation it was lower than before ligation.3. Following pylorus ligation pentagastrin and histamine stimulated the acid output in vagally intact and in acutely vagotomized but not in chronically vagotomized rats. By contrast, pentagastrin raised the histidine decarboxylase activity in vagally intact and in chronically vagotomized, but not in acutely vagotomized rats.4. The two major populations of endocrine cells of the oxyntic gland area (ECL cells and A-like cells) are argyrophil, store histamine and are capable of taking up exogenous DOPA and of decarboxylating it to dopamine which is retained in the cytoplasm for several hours. As evidenced by light and fluorescence microscopy pylorus ligation did not affect their argyrophilia or their ability to produce and store dopamine.5. Pylorus ligation caused ultrastructural changes in the gastrin cells of the pyloric gland area and in the histamine-storing ECL and A-like cells of the oxyntic gland area. The two endocrine cell types in the oxyntic gland area were enlarged by pylorus ligation, more so after 16 hr than after 4 hr. The size of the gastrin cells seemed unaffected. In all three cell types pylorus ligation reduced the number of cytoplasmic granules. There was no increase in the Golgi area or in the endoplasmic reticulum in any of the endocrine cell types of the oxyntic gland area. It appears unlikely that the ultrastructural changes of the ECL and A-like cells reflect an increased rate of histamine mobilization.6. The acid response to pylorus ligation probably reflects neuronal reflex mechanisms exclusively. There is no evidence that gastrin or histamine released from gastric endocrine cells mediate the response.

show abstract

Gastrin cell proliferation after chronic stimulation: effect of vagal denervation or gastric surgery in the rat.

Cited by 59 publications

References 29 publications

Secretion of acid, gastrin, and cobalamin‐binding proteins by the fetal pig stomach: developmental regulation by cortisol

Secretion of acid, gastrin, and cobalamin‐binding proteins by the fetal pig stomach: developmental regulation by cortisol

Reciprocal regulation of antral gastrin and somatostatin gene expression by omeprazole-induced achlorhydria.

Gastric acid response to pylorus ligation in rats: is gastrin or histamine involved?

Contact Info

Product

Resources

About