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Chapter 9 (page 35)
G cell density was found to be significantly lower along the lesser curvature and
on the anterior and posterior walls than along the greater curvature. This held true in all
patient groups excepting that of duodenal ulcer with uraemia. It was concluded that the
densest concentration of G cells occurred in the terminal antrum, i.e. the distal 3.0cm of
the stomach; that the G cell density was significantly higher along the greater than along
the lesser curvature; that individual variations existed in the antral G cell density, the
total G cell mass and the spatial distribution of G cells in the antrum; that a transitional
zone, of varying width, occurred in all patients; and that the G cell density in the distal
antrum was lower in patients with gastric ulceration than in the other patient categories.
A study by Royston et al. (l978) showed results similar to those of Stave and Brandtzaeg
(l976, l978). The highest density of G cells was found in "antral" mucosal glands near
the pylorus, the number gradually decreasing in an orad direction until the junctional
zone between antrum and corpus was reached, where a marked decrease in numbers
occurred. These authors found significant direct correlations between antral area and G
cell density, between peak acid output and G cell population, and between basal plasma
gastrin and G cell density.
G cells act in an endocrine rather than a paracrine or neurocrine way; being secreted into
the bloodstream, circulating gastrin (consisting of different molecular types) produces its
effects on distant target cells. It should therefore be looked upon as a hormone. There is
evidence that some gastrin is also secreted into the lumen, but the physiological
significance of this is not clear (Uvnäs-Wallensten l978). Gastrin or its synthetic
analogues has a number of effects on the upper gastrointestinal tract, some of the most
important being stimulation of hydrochloric acid, pepsinogen and intrinsic factor
secretion by the stomach; stimulation of bicarbonate and enzyme secretion by the
pancreas; increase in tone of the lower esophageal sphincter; increase in amplitude of
smooth muscle contractions in the stomach and jejunum (Theron and Meyer l976); and
trophic action on the fundic mucosa, pentagastrin inducing hypertrophy of the mucosa
and increases in DNA, RNA and protein synthesis (Johnson and Guthrie l976; Dockray
l978). Removal of the "antrum" leads to atrophy of the oxyntic glandular zone (Dockray
l978).
Gastrin release is induced by vagal activity, mechanical distension of the stomach, certain
food constituents, and is controlled by intra-antral pH (Uvnäs-Wallensten l978).
Acidification of antral mucosa inhibits release of gastrin and is probably an important
physiological mechanism for the control of gastrin secretion (Walsh and Grossman l975).
The kidneys and small intestine catabolise gastrin (Dockray l978).
Hypergastrinaemia is produced by the following conditions: (1) gastrinomas, which
generally arise in the pancreas, occasionally in the duodenum and only rarely in the
"antrum" (Yalow and Berson l970; Gregory and Tracy l975; Dockray l978); (2)
removal or disease of organs participating in the catabolism of gastrin, e.g. after loss of
kidney function or after extensive small bowel resection (Dockray l978); (3) pernicious
anaemia, in which the atrophic gastritis may spare the antrum and in which there is a
tendency toward hyperplasia of G cells, resulting in serum gastrin concentrations which
may be in the gastrinoma range (Yalow and Berson l970; Dockray l978). Achlorhydric
and hypochlorhydric patients also tend to have high circulating gastrin concentrations due
to diminished acid inhibition (Dockray l978); (4) increased secretion from antral G cells
(Walsh and Grossman l975).
Krulich et al. (l968, l969) and Brazeau et al (l973) isolated a tetradecapeptide from ovine,
and Schally et al (l976) from porcine hypothalamic tissue, which was shown to inhibit
release of growth hormone (GH) from the pituitary gland. Later named somatostatin, it
has subsequently been found to be widely distributed in the central nervous system
(Brownstein et al. l975; Arimura et al. l978; Forssmann et al. l979), the gastrointestinal
tract (Arimura et al. l975, l978) and other organs in experimental animals and man.
Using radioimmunoassay the distribution in rat organs other than the central nervous
system was determined (Arimura et al. l975, l978); it was shown that the pancreas had
the highest concentration, namely 34ng/mg protein, followed by the stomach with a
concentration of 12ng/mg. In the stomach the hormone was found in the pyloric and
oxyntic mucosal zones but not in the cardiac zone. The total amount in either the
pancreas or stomach was greater than in the hypothalamus; the duodenum, jejunum and
ileum contained lesser amounts, ranging from 1.2 to 1.8ng/mg protein. Other organs
such as the liver, spleen, kidneys and adrenals did not contain significant amounts.
Combined immunocytochemical and histological methods for demonstrating endocrine
granules showed that somatostatin was present in D cells in the islet system of the
pancreas (Polak et al. l975) and in morphologically similar D cells in the gastrointestinal
tract (Polak et al. l976), localized predominantly in the midzone of the mucosal glands.
According to Bloom and Polak (l978) the highest concentration of D cells occurs in the
pancreas and pyloric mucosal zone, where the incidence is more than 31 cells per mm².
In the remainder of the stomach and duodenum there are 11 to 30 cells per mm², and in
the jejunum 1 to 10 cells per mm²; in the ileum and colon the number is zero.
Somatostatin not only suppresses the secretion of growth hormone, but possesses a wide
variety of inhibitory actions on other pituitary and extra-pituitary secretions. It
suppresses the release of thyroid-stimulating hormone by the pituitary, the release of
glucagon, insulin and exocrine secretions by the pancreas, the secretion of
cholecystokinin, motilin and secretin by the intestine, and the secretion of gastrin, gastric
acid and pepsin by the stomach (Pearse et al. l977; Konturek et al. l978).
Experimental lowering of "antral" pH induces a release of somatostatin by D cells in the
pyloric mucosal zone. It appears that somatostatin suppresses gastric acid secretion by
direct action on the parietal cells of the cardiac and oxyntic mucosal zones (Arimura et al.
l978). Lowering the pH also inhibits the secretion of gastrin; consequently low pH
suppresses both gastric acid and gastrin secretion (Arimura et al. l978).
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