Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

People with anorexia (AN) and bulimia nervosa (BN) have altered patterns of eating. It is possible that alterations of the neuropeptide gastrin releasing peptide (GRP), a bombesin (BBS) -like peptide with potent central anorexigenic activity, could contribute to disturbed eating behavior. To avoid the confounding effects of pathologic eating behavior, we measured cerebrospinal fluid (CSF) GRP concentrations in women who were long-term recovered (>1 year, normal weight, and regular menstrual cycles, no binging or purging) from AN (REC AN, N=12) or BN (REC BN, N=21) compared to healthy control women (NC, N=15). CSF GRP was significantly lower (chi(2)=9.41(3), p<0.01) in REC BN (9.6+/-3.1 pg/ml) compared to NC (13.4+/-5.5 pg/ml) and REC AN (11.6+/-2.9 pg/ml). Persistent GRP abnormalities after recovery from BN raise the possibility that this alteration might be trait-related and contribute to episodic hyperphagia in BN.
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PMID:Reduced gastrin releasing peptide in cerebrospinal fluid after recovery from bulimia nervosa. 1156 53

The present study was designed to evaluate the usefulness of plasma gastrin determinations as a diagnostic aid and to review the clinical and haematological findings in cattle with bleeding abomasal ulcers. Twenty-nine cows with bleeding abomasal ulcers and six healthy cows were used. Clinical and laboratory examinations, including plasma gastrin levels, were performed. Anorexia, depression, dark-coloured to black faeces, pale mucous membranes, abdominal pain, moderate tachycardia and tachypnoca were the most pronounced clinical symptoms in the cattle with bleeding abomasal ulcers. Plasma gastrin concentration was significantly higher (P < 0.05) in the cattle with bleeding abomasal ulcers than in healthy cows. The mean plasma gastrin concentration in healthy cattle was 103.2 pg/ml, while the mean plasma gastrin concentrations in cattle with bleeding abomasal ulcers were found to be 213.6 pg/ml. Haemoglobin levels, packed cell volume, total white blood cell count and mean corpuscular volume were significantly lower (P < 0.05) in the cows with bleeding abomasal ulcer than in the healthy cattle. The results of this study show that measurement of plasma gastrin can be useful in the diagnosis of bleeding abomasal ulcers in cattle.
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PMID:Plasma gastrin activity and the diagnosis of bleeding abomasal ulcers in cattle. 1176 13

H. pylori is a major cause of primary chronic gastritis and peptic ulcer disease in children. The authors give an account of H. pylori infection (cagA+, vacA+) in a 15-year-old girl where the initial clinical features included fatigue, collapses, and anorexia, elevated serum gastrin level (> 1000 mIU/l) raised the suspicion of gastrinoma. H. pylori gastric infection was also associated with iron-deficiency anemia. After treatment for H. pylori infection (omeprazole, clarithromycin, amoxycillin), clinical symptoms improved consistently, the serum gastrin level was repeteadly quite normal and hematologic and iron profiles were within the normal range. There is compelling evidence that H. pylori must be taken into account as a cause of hypergastrinemia other than gastrinoma in childhood.
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PMID:[Hypergastrinemia associated with Helicobacter pylori infection and sideropenic anemia in a 15-year-old girl]. 1265 31

The dog of this case was a 10-year-old Shih Tzu with refractory vomiting, diarrhea and anorexia. Endoscopy revealed an unclear at gastric angle, a stenosis at pyloric antrum and congestion in duodenal mucosa. Since abnormal shadows of irregular echo-levels were disclosed by pancreas ultrasonography, serum gastrin level was determined with a suspect of gastrinoma. And an increase of serum gastrin was demonstrated. In addition, postmortem histological examination revealed that the pancreatic cells were positive for gastrin. Based on these findings, the dog was diagnosed as pancreatic gastrinoma.
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PMID:A case of canine gastrinoma. 1535 55

Hepatobiliary neuroendocrine carcinoma was diagnosed in 17 cats in a period of 10 years. Seven tumors were of intrahepatic origin, one of which was a composite containing components of epithelial and neuroendocrine carcinoma. Nine tumors were of extrahepatic origin, and one tumor was located in the gall-bladder. The cats were adult and geriatric, and the male : female ratio varied according to tumor group. Hepatomegaly, anorexia, weight loss, and vomiting were the most common clinical signs observed in the cats with hepatic neuroendocrine carcinoma. The cats with extrahepatic neuroendocrine carcinoma showed these signs plus icterus (5/9) and high concentrations of hepatic enzymes. Histologically, the hepatic neuroendocrine carcinomas had two patterns, one with acinar structures separated by vascular stroma lined by cuboidal or columnar cells and the other solid with groups of anaplastic cells separated by vascular stroma. The composite tumor consisted of both bile duct carcinoma and neuroendocrine carcinoma. The extrahepatic neuroendocrine carcinomas and the gallbladder neuroendocrine carcinoma were characterized by solid sheets or groups of round to oval cells with vascular or fibrovascular stroma. Immunohistochemical examination of 10 of the neuroendocrine carcinomas revealed that all 10 stained with neuron-specific enolase; one bile duct carcinoma and the gallbladder carcinoma stained with chromogranin; four of five bile duct carcinomas and the gall bladder carcinoma stained with synaptophysin; and one bile duct carcinoma stained with gastrin. One cat with hepatic carcinoma had duodenal ulcer; in this cat, ultrastructural studies showed neurosecretory granules leading to the diagnosis of Zollinger-Ellison syndrome. In four cats in which necropsy was permitted, carcinomatosis (4/4), lymph nodes (4/4), lungs (2/4), and intestines (1/4) were the metastatic sites. Fourteen of the 17 cats were euthanatized during or immediately after surgery.
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PMID:Hepatobiliary neuroendocrine carcinoma in cats: a clinicopathologic, immunohistochemical, and ultrastructural study of 17 cases. 1587 79

In dogs gastrinomas are rare endocrine neoplasms that have always been reported to arise from the pancreas. We report here what we believe to be the first case of a duodenal gastrinoma in a dog. A nine-year-old, male, Pekinese dog was presented with a three-day history of anorexia, vomiting and mucous diarrhoea. Clinical examination and laboratory findings suggested the presence of a severe hepatobiliary disorder. Abdominal ultrasonography showed a diffuse increase in echogenicity of the liver, with severe gallbladder dilation and marked dilation of the cystic duct, common bile duct and extrahepatic bile ducts. Based on these findings, an extrahepatic biliary tract obstruction (EBTO) of unknown cause was suspected. At laparotomy, the gallbladder and the extrahepatic bile ducts appeared severely dilated. The gallbladder was tense and could not be compressed suggesting an outflow obstruction. The duodenum at the level of the common duct orifice appeared slightly thickened and severely hardened for a length of 1 cm. Biopsies from the duodenum and liver were obtained and a cholecystoduodenostomy was performed. The duodenal biopsy revealed severe fibrosis of the submucosa and a infiltrate of small pockets and cords of round to polygonal cells with granular cytoplasm. Based on this appearance the differential diagnoses included neuroendocrine tumours and poorly differentiated carcinoma. Despite surgery and supportive therapy the dog continued to be anorexic and to vomit 3-6 times daily. After euthanasia and necropsy, histopathology showed the presence of a neuroendocrine neoplasia involving the duodenal wall with focal invasion of the adjacent pancreas and small liver metastases. On immunohistochemistry, the cytoplasm of approximately 90% of neoplastic cells intensely expressed neuron specific enolase and gastrin. These findings were consistent with a diagnosis of gastrinoma.
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PMID:Common bile duct obstruction due to a duodenal gastrinoma in a dog. 1599

Systemic infection produces a highly regulated set of responses such as fever, anorexia, adipsia, inactivity, and cachexia, collectively referred to as sickness behavior. Although the expression of sickness behavior requires immune-brain communication, the mechanisms by which peripheral cytokines signal the brain are unclear. Several mechanisms have been proposed for neuroimmune communication, including the interaction of cytokines with peripheral nerves. A critical role has been ascribed to the vagus nerve in mediating sickness behavior after intraperitoneally delivered immune activation, and converging evidence suggests that this communication may involve neurochemical intermediaries afferent and/or efferent to this nerve. Mice lacking functional CCK(2/gastrin) receptors (CCK(2)KO) and wild-type (WT) controls were administered LPS (50, 500, or 2,500 microg/kg; serotype 0111:B4; ip). Results indicate a role for CCK(2) receptor activation in the initiation and maintenance of LPS-induced sickness behavior. Compared with WT controls, CCK(2)KO mice were significantly less affected by LPS on measures of body temperature, activity, body weight, and food intake, with the magnitude of effects increasing with increasing LPS dose. Although activation of CCK(2) receptors at the level of the vagus nerve cannot be excluded, a possible role for these receptors in nonvagal routes of immune-brain communication is suggested.
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PMID:CCK(2) receptor nullification attenuates lipopolysaccharide-induced sickness behavior. 1695 66

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.
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PMID:[Physiopathological mechanisms of abomasal Trichostrongylidae infections in small ruminants]. 1717 51

The distribution and density of gastric endocrine cells in Balb/c mice bearing CT-26 carcinoma cells were studied immunohistochemically employing specific antisera against serotonin, somatostatin, glucagon, gastrin, cholecystokinin (CCK)-8 and human pancreatic polypeptide (hPP). The animals were divided into two groups, a non-implanted sham group and a CT-26 carcinoma cell-implanted group. Samples were collected from two regions of the stomach (fundus and pylorus) at 28 days after implantation of the medium or the CT-26 cells (1x10(5) cells/mouse). Five of the 6 types of immunoreactive (IR) cells were identified, with only the hPP IR cells not being detected. The regional distribution of the gastric endocrine cells in the CT-26 implanted group was similar to that of the non-implanted sham group. However, the endocrine cells were significantly decreased in the CT-26-implanted group as compared to those of the non-implanted sham group. Serotonin- and somatostatin-IR cells in the fundus and pylorus , and gastrin- and CCK-8-IR cells in the pylorus of the CT-26 implanted groups were significantly decreased compared to those of the sham group. In addition, glucagon-IR cells were restricted only to the fundus of the sham animals. hPP-IR cells were not detected in either the T-26 implanted- or the non-implanted group. Since endocrine cells are the anatomical units responsible for the production of gut hormones, a change in their density may reflect a change in their capacity to produce such hormones. Implantation of the tumor cell mass induced severe quantitative changes in gastric endocrine cell density, an abnormality which may contribute to the development of gastrointestinal symptoms, such as anorexia and indigestion, frequently encountered in cancer patients.
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PMID:Changes in gastric endocrine cells in Balb/c mice bearing CT-26 carcinoma cells: an immunohistochemical study. 1721 38

Tumors of gastrin-secreting cells (gastrinomas) result in a characteristic clinical syndrome of hypergastrinemia, which leads to gastric acid hypersecretion with subsequent severe gastrointestinal ulceration. The most common clinical signs are inappetance/anorexia, lethargy, weight loss, vomiting, diarrhea, and hypoalbuminemia. Hypergastrinemia is also seen in other disorders and caution should be used in utilizing fasting serum gastrin concentrations as the sole diagnostic criterion.
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PMID:Gastrinoma (Zollinger-Ellison Syndrome) in the Dog and cat. 1742 47


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