gastrins and Anorexia

gastrins has been researched along with Anorexia* in 6 studies

Reviews

2 review(s) available for gastrins and Anorexia

ArticleYear
[Physiopathological mechanisms of abomasal Trichostrongylidae infections in small ruminants].
    Parassitologia, 2006, Volume: 48, Issue:3

    Abomasal Trichostrongylidae infections are still today an important cause of scarce performances in small ruminants, mainly when bred in extensive systems. Although morpho-biology, symptomatology, prophylaxis and therapy of these infections are well known, other, such as physiopathology, are less investigated. The aim of the present note is to review the more important physiopathogenetic mechanisms of abomasal Trichostrongylidae infections, with special emphasis to Haemonchus spp. and Teladorsagia spp. The parasitic anorexia due to the action of gastrin, the defects of digestion due to hypocloridia, the scarce intestinal absorption and anaemia caused by H. contortus are discussed. Furthermore, the effects of hypersensitivity sometimes caused by these abomasal nematodes are examined. A better knowledge of physiopathological mechanisms can represent an important factor to understand the relationships between host and parasite, useful to set up new diagnostic techniques or new therapeutic and prophylactic protocols for sanitary education and control plans of these important and widespread parasitic infections.

    Topics: Abomasum; Anemia, Hemolytic; Animals; Anorexia; Female; Gastrins; Goat Diseases; Goats; Haemonchiasis; Haemonchus; Host-Parasite Interactions; Hypoalbuminemia; Male; Sheep; Sheep Diseases; Stomach Diseases; Trichostrongyloidea; Trichostrongyloidiasis

2006
Pathophysiology of abomasal parasitism: is the host or parasite responsible?
    Veterinary journal (London, England : 1997), 2000, Volume: 160, Issue:3

    Nematode larvae developing within the glands cause local loss of parietal cells and mucous cell hyperplasia whereas reduced acid secretion, increased serum gastrin and pepsinogen concentrations and generalized histological changes are associated with parasites in the abomasal lumen. Parietal cells with dilated canaliculi and/or degenerative changes typical of necrosis are present soon after the transplantation of adult worms, and abomasal secretion is also affected. Anaerobic bacteria survive in greater numbers as the pH rises, with bacterial densities becoming similar to ruminal populations at an abomasal pH of 4 and above. Failure to lyse bacteria may affect adversely the nutrition of the host. The parasites may initiate the pathophysiology through the release of excretory/secretory (ES) products which either act directly on parietal cells or indirectly through enterochromaffin-like (ECL) cells by provoking inflammation or by disrupting the protective mucosal defence system. Parietal cell dysfunction is proposed as a key event which leads to loss of mature chief cells and mucous cell hyperplasia, as well as hypergastrinaemia. Inflammation increases circulating pepsinogen concentrations and may also contribute to increased gastrin secretion. Stimulation of mucosal proliferation and differentiation of parietal cells in the isthmus by the raised serum gastrin levels will be beneficial by generating a new population of active parietal cells and adequate acid secretion.

    Topics: Abomasum; Animals; Anorexia; Bacteria, Anaerobic; Cattle; Cattle Diseases; Gastrins; Haemonchiasis; Haemonchus; Host-Parasite Interactions; Hydrogen-Ion Concentration; Intestinal Mucosa; Ostertagia; Ostertagiasis; Pepsinogens; Sheep; Sheep Diseases; Stomach Diseases

2000

Other Studies

4 other study(ies) available for gastrins and Anorexia

ArticleYear
Vagal and splanchnic afferent nerves are not essential for anorexia associated with abomasal parasitism in sheep.
    Veterinary parasitology, 2006, Feb-18, Volume: 135, Issue:3-4

    Heavy burdens of the abomasal nematode, Ostertagia (Telodorsagia) circumcincta, in growing lambs result in a reduction in liveweight gain due largely to a drop in voluntary feed intake. The present study investigated: (1) the role of subdiaphragmatic vagal and non-vagal visceral afferent nerves in mediating a reduction in voluntary feed intake, using subdiaphragmatic vagal deafferentation (vagotomy) either alone or in combination with coeliac-superior mesenteric ganglionectomy (vagotomy and sympathectomy); and (2) the association between appetite, abomasal pH, selected blood values (amidated gastrin (G-17-amide), glycine-extended gastrin (G-17-Gly), pepsinogen and leptin) and worm burden, in sheep experimentally infected with 100,000 O. circumcincta infective larvae per os. Neither vagotomy alone nor vagotomy and sympathectomy in combination adversely affected the establishment or course of development of the parasite burden, when compared with a control group subject to sham surgery. Furthermore, neither surgical procedure prevented the drop in appetite seen 5-10 days post-infection, although combined vagotomy and sympathectomy did reduce voluntary feed intake prior to the start of the study. Ostertagia infection resulted in a significant increase in abomasal pH in all three groups, which was accompanied by an increase in blood G-17-amide and in G-17-Gly, the latter reported for the first time in parasitized ruminants. There were no significant differences in blood leptin, also reported for the first time in parasitized sheep, either between groups or in comparison with pre-infection levels, though weak negative correlations were established between blood leptin and appetite from day 5 to the end of the study in all three groups and a positive correlation with blood G-17-amide in the control group over the same period. These data suggest that neither intact subdiaphragmatic vagal afferent nerves or coeliac-superior mesenteric ganglion fibres, nor changes in circulating gastrin and leptin concentrations play a major role in mediating the hypophagic effects of O. circumcincta in parasitized sheep.

    Topics: Abomasum; Afferent Pathways; Animals; Anorexia; Energy Intake; Female; Gastrins; Hydrogen-Ion Concentration; Leptin; Male; Ostertagiasis; Random Allocation; Sheep; Sheep Diseases; Sympathectomy; Time Factors; Vagotomy; Weight Gain

2006
Function and regulation of cholecystokinin octapeptide, beta-endorphin and gastrin in anorexic infantile rats treated with ErBao Granules.
    World journal of gastroenterology, 2001, Volume: 7, Issue:2

    To study the role of cholecystokinin octapeptide (CCK-8),beta endorphin (beta EP), and gastrin in an anorexic infantile rat model and no subsequent regulation of nose peptides by the Yunpi complex prescription ErBao Granule.. We fed infantile rats with special prepared forage. A liquid extract of ErBao Granule was administered to the rats daily for 3 weeks, CCK-8, beta-EP, and gastrin concentrations in hypothalamus, gastric antrum, and plasma of the rats were measured by radioimmunoassay, and were compared with controls.. Treatment of rats with ErBao Granule inhibited CCK-8 secretion and increased beta-EP and gastrin secretion. CCK-8 concentration in hypothalamus and plasma of model control group increased significantly and correlated negatively with food intake of models, respectively. beta-EP concentration in gastric antrum and plasma of model control group decreased significantly and showed a positive correlation with food intake of models, respectively. Hypothalamus concentration of beta-EP was similar in models and controls. Gastrin concentration in gastric antrum of models was lower than in the blank control group, and correlated positively to food intake of models. Finally, CCK-8 concentrations in plasma of rats showed a positive correlation with plasma beta-EP (r=-0.68, P<0.05).. The increased plasma and hypothalamus concentration of CCK-8, decreased gastric antrum and plasma level of beta-EP, and decreased gastric antrum concentration of gastrin are associated significantly with the anorexia of infantile anorexic rat models produced by special for-age. ErBao Granule can reverse these changes, which may be the major mechanisms of ErBao Granule simulating feeding.

    Topics: Animals; Anorexia; beta-Endorphin; Diet; Female; Gastrins; Hypothalamus; Male; Models, Animal; Pyloric Antrum; Rats; Rats, Sprague-Dawley; Sincalide

2001
The dissociation of tumor-induced weight loss from hypoglycemia in a transplantable pluripotent rat islet tumor results in the segregation of stable alpha- and beta-cell tumor phenotypes.
    Endocrinology, 1993, Volume: 133, Issue:5

    We previously established pluripotent transformed rat islet cell lines, MSL-cells, of which certain clones have been used to study processes of islet beta-cell maturation, including the transcriptional activation of the insulin gene induced by in vivo passage. Thus, successive sc transplantation in NEDH rats resulted in stable hypoglycemic insulinoma tumor lines, such as MSL-G2-IN. Occasionally, hypoglycemia as well as severe weight loss were observed in the early tumor passages of MSL-G and the subclone, NHI-5B, which carry the transfected neomycin and human insulin genes as unique clonal markers. By selective transplantation, it was possible to segregate stable anorectic normoglycemic tumor lines, MSL-G-AN and NHI-5B-AN, from both clones. These tumors cause an abrupt onset of anorexia when they reach a size of 400-500 mg (< 0.3% of total body weight), and the observed weight loss parallels that of starved rats until death results from cachexia. After tumor resection, animals immediately resume normal feeding behavior. Comparative studies of hormone release and mRNA content in anorectic lines, MSL-G-AN and NHI-5B-AN, vs. those in the insulinoma line, MSL-G2-IN, revealed selective glucagon gene expression in both of the anorectic tumors, whereas insulin and islet amyloid polypeptide gene expression were confined to the insulinoma. Both tumor phenotypes produced cholecystokinin and gastrin in variable small amounts, making it unlikely that these hormones contribute to the anorectic phenotype. Tumor necrosis factor (cachectin) was not produced by any of the tumors. Proglucagon was processed as in the fetal islet to products representative of both pancreatic alpha-cell and intestinal L-cell phenotypes, with glucagon and Glp-1 (7-36)amide as the major extractable products. In contrast to the administration of cholecystokinin, neither glucagon, Glp-1 (7-36)amide, nor their combination, affected feeding behavior in fasted mice, suggesting the presence of a hitherto unidentified anorectic substance released from the glucagonoma. We conclude 1) that glucagonomas and insulinomas can be derived from a common clonal origin of pluripotent MSL cells, thus supporting the existence of a cell lineage relationship between islet alpha- and beta-cell during ontogeny; and 2) that our glucagonomas release an anorexigenic substance(s) of unknown nature that causes a severe weight loss comparable to that reported in animals carrying tumor necrosis factor-producing experimental

    Topics: Adenoma, Islet Cell; Animals; Anorexia; Base Sequence; Blotting, Northern; Cholecystokinin; Eating; Gastrins; Gene Expression; Glucagon; Hormones; Hypoglycemia; Molecular Sequence Data; Neoplasm Transplantation; Pancreatic Neoplasms; Protein Precursors; Rats; Tumor Cells, Cultured; Weight Loss

1993
Serum levels of gastrin, insulin and glucagon as possible factors of anorexia in pigs infected once with Ascaris suum.
    Veterinary parasitology, 1990, Volume: 36, Issue:3-4

    In order to determine possible mediators for development of anorexia in pigs infected with Ascaris suum, serum levels of gastrin, insulin and glucagon were measured. After a single high oral dose of 100,000-200,000 embryonated eggs the serum levels of gastrin and insulin in the infected pigs did not significantly differ from those in controls. Serum glucagon levels in the infected groups, however, were lower than those in controls and the difference was more evident 24 days postinoculation and later.

    Topics: Animals; Anorexia; Ascariasis; Feeding and Eating Disorders; Female; Gastrins; Gastrointestinal Hormones; Glucagon; Insulin; Male; Radioimmunoassay; Reproducibility of Results; Swine; Swine Diseases

1990