Endocrine Profile in Rats with Postgastrectomy Malabsorption: a Pilot Study

Abnormal endocrine profile, especially in the enteropancreatic axis, was described in rats with malnutrition caused by malabsorption after total gastrectomy. Insulin, substance P and motilin concentrations at the fasting condition were significantly elevated in malnutritious rats after total gastrectomy when compared to those in control rats. A significant elevation of pancreatic glucagon and motilin was noted after intraduodenal fat administration in malnutritious rats. These data suggest that these peptides of many humoral factors may thus cause abnormal enteropancreatic axis and consequent malnutrition

Preventive Effect of Proglumide on Erosive Gastritis in the Rat

The purpose of this study is to determine whether or not proglumide has a preventive effect on the erosive gastritis induced by sodium salt of taurocholic acid (TCA) in the rat. Its effect on the formation of gastric erosions, serum gastrin levels and secretion of acid and pepsin were also studied. The rats were given standard feed containing 0.25% proglumide and water containing 5mM TCA (experimental E group). The control rats were given standard feed and water containing 5mM TCA (TCA group). All rats were killed at the end of the 3 months. The tissue specimens of the resected gastric mucosa were stained with hematoxylin eosin for histopathology and with azan for evaluation of fibrous ploriferation. From microscopic observation of the stained specimens, the following results were obtained. TCA-group showed long mucosal surface injury (erosion), inflammatory cell infiltration, a reduction in the number of parietal cells, a decrease of mucosal thickness, and proliferation of collagenous fiber. In contrast, in the E group, these morphological and morphoquantitative changes were significantly small. The length of erosion and inflammatory cell infiltration were significantly reduced in the E group when compared with the TCA group. Furthermore, mucosal thickness was almost normal and fibrous proliferation was significantly scarce in the E group. Proglumide had an insignificant effect on pH on the mucosa, volume and pH of gastric juice, serum gastrin levels and tetragastrin-induced secretion of acid and pepsin. It is, thus, evident that proglumide has a preventive effect on the induction of erosive gastritis caused by TCA in the rats. Since it is difficult to explain its mechanism for the prevention of gastritis from only the already known facts that it has protective action on gastric mucosa and an inhibitory effect on secretion of acid and pepsin, unknown mechanisms are suspected to be involved

A Galanin-Like Peptide in the Colon of the Golden Hamster

Galanin-like immunoreactive peptide was studied in the colonic wall of the golden hamster using the immunoflurescent technique. Galanin-like immunoreactivity was observed mainly in cell bodies of the myenteric plexus and in fibers in the lamina propria mucosae and in the circular muscle layer. The submucosal plexus and submucosal connective tissue, however, contained very little galanin-like immunoreactive peptide. This peptide appears to be instrinsic mainly to the colon. The presence of the peptide indicates some possible biological roles in the colonic function

Induction of Experimental Atrophic Gastritis by N-Methyl-N'-Nitro-N-Nitrosoguanidine or Taurocholic Acid in Donryu Rats

The morphology of the rat (Donryu) gastric mucosa was examined by light microscopy after administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or taurocholic acid (TCA), a component of bile acids. MNNG was given to rats ad libitum from light-sealed bottles for 5 months and deionized water was given freely for 6 months thereafter. TCA was administered to rats freely for 11 months. Deionized water was given to rats as control (non-treated rats). Rats treated with MNNG or TCA and control rats were killed at 11 months after the beginning of the experiment. Using 3 micron tissue samples taken from the area of the gastric mucosa designated before the experiment, hematoxylin and eosin and azan stain were made for histopathological evaluation and fibrosis. Marked atrophic changes, such as reduction in the number of parietal cells, shortened mucosa! length, inflammaotry cell infiltration, and proliferation of fibrosis, were present in the gastric mucosa of rats treated with MNNG as well as TCA. These findings were typical for atrophic gastritis. Such atrophic changes were slight in the gastric mucosa of the control rats. The frequency of tumourous lesions was very low in MNNG-treated rats. We have concluded on the basis of the present data that MNNG as well as TCA can induce atrophic gastritis in Donryu rats

Existence of VIP and PHI-Like Immunoreactivities in the Amphibian Gut

The present paper provides the first definitive evidence on the presence and possible co-existence of VIP- and PHI-like peptides in the peripheral nervous system of the amphibian (bullfrog) gut wall. The possibility of co-existence of the peptides suggests that VIP- and PHI-like peptide may be synthesized from the same precursor protein in the amphibian

Gastrin and Somatostatin in Patients with Hyperchlorhydric Duodenal Ulcer

Hormonal and morphological studies were conducted to ascertain the role played by gastrin and somatostatin in the pathophysiology of duodenal ulcer, in particular hyperchlorhydric duodenal ulcer, using 35 patients with duodenal ulcer, of whom 15 were hyperchlorhydric and 20 were normochlorhydric. Twenty normal subjects with normochlorhydria were used as a control. In patients with hyperchlorhydric duodenal ulcer following significant findings were observed: 1. Basal and stimulated hyperchlorhydria, 2. Parietal cell hyperplasia, 3. Basal hypergastrinemia, 4. Increased concentration of gastrin and large number of G cells (G cell hyperplasia) in the antral mucosa. 5. Mucosal concentration of somatostatin and D cells in the antrum was reduced, but the former in patients with hyperchlorhydric duodenal ulcer was not different from that in patients with normoacidic duodenal ulcer. 6. A significant correlation in mucosal concentration was demonstrated between gastrin and somatostatin in control subjects but not in patients with duodenal ulcer. 7. There was a significant correlation in maximal acidity in gastric secretion and mucosal concentration of antral somatostatin in control subjects but not in patients with duodenal ulcer. 8. Concentration of plasma somatostatin in patients with duodenal ulcer was not different from that in control subjects. These findings indicate that gastrin and somatostatin may participate in the pathophysiology of duodenal ulcer, at least in the subgroup of duodenal ulcer associated with hyperchlorhydria, and the subgroup of duodenal ulcer may be an endocrine disorder

実験胃炎・胃粘膜の GEP ホルモン細胞動態

The aim of this study was to ascertain the morphological changes in the endocrine cell profile in the atrophic mucosa of mice with autoimmune gastritis induced by neonatal thymectomy and administration of carcinogenic chemical, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Proliferation of argyrophil cells, gastrin (G17, G34) cells in areas of pseudopyloric metaplasia, enteric hormone (GIP, secretin, substance P, enteroglucagon) containing cells and enterochromaffin cells in areas of intestinal metaplasia of the atrophic mucosa was observed in mice with autoimmune gastritis together with proliferation of enterochromaffin-like cells and undifferentiated endocrine cells in their atrophic mucosa. These findings suggest that atrophic mucosae, especially epithelia of pseudopyloric and intestinal metaplasia as well, have the potential of producing endocrine cells which are normally present in the gastric antrum and intestine

Early Changes in the Gastric Mucosa with MNNG Exposure in the Rat

The morphology of the rat gastric mucosa was examined by light microscopy after short term-administration of a carcinogenic agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG, at a dose of 50 mg/I in 0.04% of Tween 60), which was given to rats ad libitum from light-sealed bottles for 3 months. Tween 60 (0.04%) was given to rats as control for 3 months. Rats thus treated were sacrificed by decapitation at the end of 3 months after the beginning of the experiment. Tissue samples were taken from the area of the gastric mucosa designated before the experiment. Tissue sections three microns in thickness were stained with hematoxylin and eosin for histopathological evaluation and stained with azan for evaluation of proliferation of collagenous fiber. Slight atrophic changes, such as reduction in the number of parietal cells per unit area (78.8 ± 15.4 in the MNNG group and 110.1 ± 20.8 in the control group), shortened mucosal thickness (5.36 ± 0.69 in the MNNG group and 6.72 ± 0.53 in the control group), slight infiltration (grade 1) of inflammatory cell infiltration, and also slight proliferation (grade 1) of collagenous fibers were present in the fundic mucosa of rats treated with MNNG, while mucosal changes of hyperplastic gastritis, such as hyperplastic glands, increased mucosal thickness (2.77 ± 0.15 in the MNNG group; 2.64 ± 0.21 in the control group), and mild infiltration (grade 2) of inflammatory cells, and mild proliferation (grade 2) of collagenous fibers were present in the pyloric mucosa of rats treated with MNNG. Furthermore, in the pyloric mucosa, focal and diffuse lesions composed of atypical cells with erosions considered to be precancerous stage were present. Diffuse mucosal surface injuries (erosions) existed in both the fundic and pyloric mucosa. Development of gastric cancer does not seem to be involved in the background such as mucosa with atrophic gastritis but with hyperplastic gastritis in short term administration of MNNG