gastrins and Taeniasis

gastrins has been researched along with Taeniasis* in 4 studies

Other Studies

4 other study(ies) available for gastrins and Taeniasis

ArticleYear
Retarded gastric acid secretion in rats infected with larval Taenia taeniaeformis.
    Parasitology research, 2002, Volume: 88, Issue:9

    The influence of hepatic larval Taenia taeniaeformis infection on gastric acid secretory activity and gastric mucosal integrity was investigated. After 12 weeks of infection with 2,000 T. taeniaeformis eggs, the gastric pH values of control and infected rats were 4.1+/-0.6 (mean +/- SD) and 8.4+/-0.2, respectively. There was no difference in the basal acid secretion between control (1.7+/-0.7 micro Eq.H(+)/15 min) and infected (1.9+/-0.3) rats. However, infected rats failed to respond to histamine stimulation, the maximum acid output level being 2.8+/-0.4 in the infected rats, compared to 12.9+/-3.3 in control rats. Larval T. taeniaeformis infection resulted in the suppression of gastric acid secretion leading to hypergastrinemia.

    Topics: Animals; Cats; Female; Gastric Acid; Gastric Mucosa; Gastrins; Histocytochemistry; Hydrogen-Ion Concentration; Parasite Egg Count; Rats; Rats, Inbred F344; Taenia; Taeniasis

2002
Hyperplasia of gastric mucosa in donor rats orally infected with Taenia taeniaeformis eggs and in recipient rats surgically implanted with the larvae in the abdominal cavity.
    Parasitology research, 1999, Volume: 85, Issue:6

    Rats heavily infected with Taenia taeniaeformis larvae in the liver show a remarkable increase in their stomach weight, hyperplasia, and hypergastrinemia. However, it is unknown what causes these phenomena. Hence, as a preliminary study to investigate the importance of larval parasitism in the liver, two experiments were done. In the first experiment, 14 donor rats were orally inoculated with 3,000 T. taeniaeformis eggs. In the second experiment, 136-300 of the larvae obtained from the rats were surgically implanted into the abdominal cavity of 7 recipient rats. Gastrin levels and histopathological changes in the gastric mucosa were investigated. In all, 11 donor rats showed hypergastrinemia and hyperplasia, 5 recipient rats showed gastric mucosal hyperplasia accompanied by excessive mucous cell proliferation, and 2 recipient rats showed hypergastrinemia. These results suggest that parasitism of the liver by the larvae is not essential for the development of hyperplasia and that factors from the larvae might cause these phenomena.

    Topics: Animals; Gastric Mucosa; Gastrins; Hyperplasia; Larva; Liver; Male; Peritoneal Cavity; Rats; Rats, Wistar; Taenia; Taeniasis

1999
Taenia taeniaeformis: gastrointestinal hyperplasia in chronically infected rats.
    Experimental parasitology, 1983, Volume: 55, Issue:2

    Topics: Animals; Cell Count; Chronic Disease; Colon; Duodenum; Esophagus; Female; Gastric Mucosa; Gastrins; Hyperplasia; Intestinal Mucosa; Intestine, Small; Intestines; Mast Cells; Organ Size; Rats; Splenomegaly; Stomach; Taeniasis

1983
Hyperplastic gastropathy in the rat due to Taenia taeniaeformis infection: parabiotic transfer and hypergastrinemia.
    Gastroenterology, 1981, Volume: 80, Issue:4

    Development of the cestode parasite Taenia taeniaeformis in the liver of rats results in gross hyperplastic changes in the stomach and small intestine. In this study we investigated the mechanism by which these lesions are induced. Acutely infected rats were joined surgically to syngeneic noninfected partners in parabiosis. When hyperplastic gastropathy developed in those rats with heavy hepatic infections with cestodes, it also occurred in the uninfected partners of the parabiotic pairs. Gastric changes were usually more severe in the uninfected partner. Duodenal mastocytosis developed in both partners, even when parasite burdens were light in the infected rats. intact chronically infected rats with hyperplastic gastropathy developed markedly elevated serum levels of the hormone, gastrin (approximately 30-fold greater than normal). When rats were antrectomized 24-48 h after infection, gastric hyperplasia still developed, but hypergastrinemia was prevented or was of only moderate degree. There was no correlation between serum gastrin levels and the degree of gastrointestinal change in the intact rats, but hypergastrinemia never developed in infected animals which did not show hyperplasia in the stomach or intestine. When infected rats were bled serially over the first 100 days of infection, hypergastrinemia developed abruptly between 50 and 60 days after infection. These results suggest that the alterations in serum gastrin levels were secondary to the development of hyperplastic changes in the gastrointestinal tract of infected rats. The primary stimuli for both the hyperplasia and the hypergastrinemia remain unknown.

    Topics: Animals; Gastrins; Hyperplasia; Parabiosis; Rats; Stomach Diseases; Taeniasis

1981