Hypergastrinaemia produces trophic effects in stomach but not in pancreas and intestines

Håkanson, R.; Blom, Håkan; Carlsson, Enar; Larsson, Håkan; Ryberg, B.; Sundler, F.

doi:10.1016/0167-0115(86)90041-8

Cited by 130 publications

(70 citation statements)

References 11 publications

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“…Thus, hypergastrinemia causes growth of the mucosa in the oxyntic gland area. Such increased growth has also been found during long-term omeprazole treatment of rats (7,15,16). Increases of a similar magnitude have also been found after long-term treatment with the H,-antagonists metiamide and cimetidine ( 5 , 1 I).…”

Section: General Tropliic Eflects Of Hypergastriiieniiasupporting

confidence: 57%

“…Plasma gastrin levels have been determined in freely-fed female rats after omeprazole at 40 or 400 pmol/kg given orally for up to 20 weeks (7,16). After the first dose, there was a rise in plasma gastrin levels, which upon prolonged treatment increased to a steady-state level.…”

Section: The Gastrin Hypothfsismentioning

confidence: 99%

“…In the dog treated with omeprazole (80 pm?l/kg, PO) for 1 year, a 50% or less increase in endocrine cell (argyrophil cell) density was observed (6), although this treatment yielded gastrin levels (22) comparable to those found in the rat during high-dose omeprazole treatment. This is to be compared with the 3-and 5-fold increases in ECL-cell number seen in rats with a similar degree of hypergastrinemia after 10 and 20 weeks treatment, respectively (7,15) (Fig. 5).…”

Section: Species Differencesmentioning

confidence: 99%

“…Apart from being a potent gastric acid secretagogue, it has a general trophic effect on the stomach (7,13,14). Thus, hypergastrinemia causes growth of the mucosa in the oxyntic gland area.…”

Section: General Tropliic Eflects Of Hypergastriiieniiamentioning

confidence: 99%

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Omeprazole: Its Influence on Gastric Acid Secretion, Gastrin and ECL Cells

et al. 1988

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The H+,K+-ATPase inhibitor omeprazole is a highly effective gastric antisecretory agent, both in animals and man, with a long duration of action. These properties are shared by a number of recently described histamine H,-receptor antagonists. In life-long oncogenicity studies of these H,-receptor antagonists, as well as with the H+,K+-ATPase inhibitor omeprazole, gastric enterochromaffin-like cell (ECL cell) hyperplasia and carcinoids have been found. The purpose of this paper is to summarize available evidence for the "Gastrin Hypothesis" to explain the development of ECL-cell hyperplasia. The hypothesis may be outlined as follows: 1) Inhibition of gastric acid secretion leads to elevated antral pH and, secondarily, to release of gastrin from the antral gastrin cells into the blood stream. 2) Gastrin causes both general hypertrophy of the oxyntic mucosa and hyperplasia of the ECL cells in the oxyntic mucosa. That this sequence of events occurs not only with omeprazole but also with other effective gastric antisecretory agents has been verified in the rat by giving the H,-receptor antagonist ranitidine as a continuous infusion. Ranitidine caused a hypergastrinemia of a similar magnitude as that seen after omeprazole, provided that the acid secretion was inhibited to a similar degree. At similar gastrin levels, ECL-cell hyperplasia of the same magnitude developed during both ranitidine and omeprazole treatment. Antrectomy prevented the development of ECL-cell hyperplasia during omeprazole treatment, indicating that the hyperplasia was not due to the drug treatment per se, but rather to the hypergastrinemia. Both the hypergastrinemia and the ECL-cell hyperplasia were found to be reversible. Control plasma gastrin levels were reached within a few days of stopping long-term treatment, and the ECL-cell density was back to normal 20 weeks after discontinuing 10 weeks of treatment with highdose omeprazole. We conclude from these studies that the ECL-cell hyperplasia seen in rats after long-term treatment with gastric acid secretion inhibitors is reversible and secondary to the hypergastrinemia, and is not caused by the drugs per se. Furthermore, although the gastrin mechanism for the regulation of the ECL cells seems to be similar in different species, there are quantitative differences with regard to the ECLcell density and possibly also the sensitivity of ECL cells to gastrin.

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Section: General Tropliic Eflects Of Hypergastriiieniiasupporting

confidence: 57%

Section: The Gastrin Hypothfsismentioning

confidence: 99%

Section: Species Differencesmentioning

confidence: 99%

Section: General Tropliic Eflects Of Hypergastriiieniiamentioning

confidence: 99%

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Omeprazole: Its Influence on Gastric Acid Secretion, Gastrin and ECL Cells

et al. 1988

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“…Studies have shown that amidated gastrins have no stimulatory effect on colon mucosal growth or progression of colon cancer in different experimental models (Hakanson et al, 1986(Hakanson et al, , 1988. Others demonstrated that non-amidated gastrins, including progastrin and Glygastrin, have a mitogenic effect on the colonic mucosa in transgenic mice (T.C.…”

Section: Cancer In Experimental Animalsmentioning

confidence: 99%