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

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

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

胆のう疾患のVIP神経

The immunocytochemical distribution of vasoactive intestinal peptide (VIP) was studied in healthy and diseased regions of the human gall bladder wall obtained after operation for cholelithiasis. Ganglionated plexuses containing VIP-like immunoreactive nerves and fibers were located in the subepithelial and muscle layer of the normal region, suggesting that VIP may exert gall bladder function, while such ganglionated plexuses were almost absent, being replaced by inflammatory cells and fibrotic tissue. This suggests that the lack of VIP may be one of the causes in the pathogenesis of gall bladder dysfunction in the case of cholelithiasis associated chronic cholecystitis

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

実験胃炎の組織化学的電子顕徴鏡的研究

Experimental gastritis was produced in BALB/c (? / +) mice by the method of neonatal thymectomy. This atrophic gastritis was confined to the gastric fundobody mucosa and spared antrum. The morphological changes in the gastric mucosa of this type of gastritis have been described in detail during the growth process after thymectomy (1, 2, 3, 6, 10, and 15 months). The mucosal changes developed from the second months after thymectomy, which were characterized by destruction and degeneration of both the parietal and chief cells in the deep glands of gastric fundobody mucosa associated with cellular infiltration in the lamina propriae. From 3 to 6 months after the1 operation, however, the structure of the whole fundobody glands became composed of mostly immature cells and mucus-containing cells. These cells were similar in appearance to mucous neck cells of the normal stomach and stained positive with PAS-alcian blue at pH 2.5. At the ultrastructural level, however, the size, electron density and number of secretory granules of mucus-containing cells were different from those of cells of the normal stomach. During this period, both parietal and chief cells were markedly decreased in number and both cells were very immature. With growth (10 to 15 months after the operation), the mucosal thickness increased, although the cells composing the glands were essentially the same as those at the early to middle stages after the operation. Thus, this type of gastritis was characteristic of fundobody-confined atrophic gastritis associated with immature and undifferentiated cells as well as mucus-containing cells and hypertrophic mucosae. These peculiar changes in the gastric mucosae increased with growth after thymectomy. The precise mechanism of induction of this type of gastritis still remains to be defined. However, first, the mucosal destruction and increased cellular proliferation are one of the possible causes, and secondly, unknown inhibitory mechanism for maturing immature cells can participate in the development of this type of gastritis. This is the other possible cause

糖尿病ラットの消化管における VIP 作動神経

Diabetic gastroenteropathy developed in about 70% of the rats with diabetes induced by streptozotocin. These rats were associated with diarrhea, gastric paresis, and small intestinal stasis. About 30% of the rats with diabetic gastroenteropathy had narrowed and contracted segments of the lower esophagus and 70% of the colon of the rats showed dilated and contracted segments. Changes in the distribution of VIP-like immunoreactivities in nerve plexuses of the gastrointestinal wall which were observed with destruction of the autonomic nerves (both submucosal and myenteric plexuses) could be one of the plausible causes of diabetic gastroenteropathy induced by streptozotocin, although the precise mechanism of the development of diabetic gastroenteropathy in rats remains obscure

Experimental Model of Gastritis Induced by Sodium Taurocholate in Rats

Experimental gastritis was produced in rats by administration of sodium taurocholate (5 mM) for 3 months. The gastritis was associated with mucosal surface injury (erosion), inflammatory cell infiltration and proliferation of interstitial fibrosis in the gastric mucosa. The number of parietal cells per unit area and the mucosal thickness, however, were not different from those in the normal mucosa, indicating that this kind of gastritis was not atrophic but erosive gastritis. The model of erosive gastritis is most useful in studies on gastroprotection and various drugs