Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropeptide Y (NPY) and somatostatin immunoreactivities are present in neural lobe axons of the rat pituitary. Both peptides are upregulated during lactation, because NPY gene expression increases in the hypothalamus and plasma concentrations of somatostatin are elevated. However, the effects of lactation on NPY and somatostatin in the neural lobe are unknown. Although NPY immunoreactivity increases in the neural lobe following salt loading of male rats, the somatostatin response is unknown. To answer these questions, NPY and somatostatin immunoreactivities in the neural lobe were examined during lactation and salt loading using immunohistochemistry and image analysis. On day 2 of lactation, the area covered by immunoreactivity, a combined measurement of axon density and size of axonal swellings, of both NPY and somatostatin increased compared to ovariectomized rats. The increase in NPY was four- to fivefold greater than that of somatostatin. By day 10 of lactation, values returned to those of ovariectomized rats. Following 10 days of salt loading, the area covered by NPY immunoreactivity increased approximately 10-fold over control male rats, whereas somatostatin remained unchanged. NPY and somatostatin were not colocalized in neural lobe axons in either paradigm, demonstrating that two different neuronal populations were involved in both cases. These data indicate that NPY and somatostatin were regulated similarly during lactation, but differentially following salt loading.
 ...
PMID:Lactation and salt loading similarly alter neuropeptide Y, but differentially alter somatostatin, in separate sets of rat neural lobe axons. 935 64

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.
 ...
PMID:How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. 939 59

It is unclear why Helicobacter pylori produces different diseases in different persons. High and low acid secretion rates probably contribute to duodenal ulceration and gastric carcinogenesis, respectively. Both of these changes seem to be corrected by eradicating Helicobacter pylori. We are therefore exploring the basic mechanisms and asking why patients react differently? Helicobacter pylori products and certain cytokines released in Helicobacter pylori gastritis release gastrin from G-cells but inhibit parietal cells. Also tumour necrosis factor alpha inhibits somatostatin-cells and interleukin 1 beta inhibits enterochromaffin-like cells. The net result is that antral gastritis tends to increase, whilst corpus gastritis tends to decrease acid secretion. Corpus atrophy further lowers acid through loss of parietal cells. Factors postulated to increase corpus gastritis include host genetics, early acquisition of Helicobacter pylori, more aggressive strains, poor general health and diets high in salt or lacking in antioxidant vitamins. Further research should address the interaction of bacterium, host and environment with a view to preventing the serious clinical outcomes.
 ...
PMID:Host mechanisms: are they the key to the various clinical outcomes of Helicobacter pylori infection? 947 95

Despite advances in endoscopic management, variceal bleeding is still associated with a significant mortality. In recent years, several therapeutic agents have been shown to lower the portal pressure and reduce variceal bleeding. In patients presenting with acute variceal bleeding, the drug of choice is somatostatin; it is as effective as endoscopic treatment and is virtually free of side-effects. The second-line drug therapy in acute variceal bleeding is a combination of vasopressin and nitroglycerine. Every patient with a history of variceal bleeding is at an increased risk of rebleeding and should receive some form of preventive therapy. In these patients, non-selective beta-blockers and endoscopic treatment are equally effective and either modality can be used. Since each episode of variceal bleeding carries a 30%-50% risk of death, cirrhotics who have never experienced variceal bleeding but are at high risk to develop this complication (high portal pressure, variceal grade III and IV, and presence of red wale markings over the varices) should be identified and treated. Beta-blockers are the treatment of choice and should be continued for the rest of the patient's life. Isosorbide-5-mononitrate is also useful in lowering the portal pressure and may be combined with beta-blockers in those who do not respond to the use of beta-blockers alone. However, isosorbide-5-mononitrate should not be given alone for a long duration because of its adverse haemodynamic effects. Additional measures which are useful in decreasing the risk of variceal bleeding are good control of ascites, especially with spironolactone and a low salt diet, and early recognition and treatment of bacterial infections.
 ...
PMID:Drug treatment of portal hypertension. 980 74

Tham et al. show that Helicobacter pylori infection lowers the density of immunoreactive somatostatin cells (D-cells) in the antral mucosa and elevates plasma gastrin concentrations. According to current hypothesis, the lack of inhibition by somatostatin allows excessive release of gastrin, which stimulates acid secretion and thus causes duodenal ulcers. The cytokine tumour necrosis factor-alpha which is released in H. pylori gastritis inhibits D-cells in culture and may be responsible. Why do not all infected persons get duodenal ulcers? Recent work shows that more aggressive strains of H. pylori have greater effects on somatostatin/gastrin physiology. Another variable is whether the infection causes corpusitis or not. Inflammation of the gastric corpus diminishes acid secretion, which greatly decreases the likelihood of duodenal ulcers but increases the risk of gastric cancer. Factors which promote corpusitis include diets with high salt content or lacking in antioxidant vitamins. Work in this area is elucidating how H. pylori causes different diseases. Hopefully this will allow us to predict and prevent its serious sequelae.
 ...
PMID:Helicobacter pylori and somatostatin cells. 985 43

Helicobacter pylori plays major causative roles in peptic ulcer disease and gastric cancer. Elevated acid secretion in patients with duodenal ulcers (DUs) contributes to duodenal injury, and diminished acid secretion in patients with gastric cancer allows carcinogen-producing bacteria to colonize the stomach. Eradication of H. pylori normalizes acid secretion both in hyper-secreting DU patients and hypo-secreting relatives of gastric cancer patients. Therefore, we and others have asked how H. pylori causes these disparate changes in acid secretion. H. pylori gastritis more or less restricted to the gastric antrum in DU patients is associated with increased acid secretion. This is probably because gastritis increases release of the antral acid-stimulating hormone gastrin and diminished mucosal expression of the inhibitory peptide somatostatin. Bacterial products and inflammatory cytokines including TNFalpha may cause these changes in endocrine function. Gastritis involving the gastric corpus tends to diminish acid secretion, probably because bacterial products and cytokines including IL-1 inhibit parietal cells. Pharmacological inhibition of acid secretion increases corpus gastritis in H. pylori-infected subjects, so it is envisaged that gastric hypo-secretion of any cause might become self-perpetuating. H. pylori-associated mucosal atrophy will also contribute to acid hypo-secretion and is more likely in when the diet is high in salt or lacking in antioxidant vitamins. Data on gastric acid secretion in patients with esophagitis are limited but suggest that acid secretion is normal or slightly diminished. Nevertheless, H. pylori infection may be relevant to the management of esophagitis because: (i) H. pylori infection increases the pH-elevating effect of acid inhibiting drugs; (ii) proton pump inhibitors may increase the tendency of H. pylori to cause atrophic gastritis; and (iii) successful eradication of H. pylori is reported to increase the likelihood of esophagitis developing in patients who had DU disease. Points (ii) and (iii) remain controversial and more work is clearly required to elucidate the relationship between H. pylori, acid secretion, gastric mucosa atrophy and esophagitis.
 ...
PMID:Helicobacter pylori modulation of gastric acid. 1078 May 81

To elucidate the role of intermediate filament proteins in endocrine cells, we investigated the expression and subcellular distribution of GFAP in mouse islets of Langerhans. For this purpose, combined immunocytochemical and biochemical analysis with a panel of antibodies was carried out to identify GFAP-immunoreactive cells in mouse endocrine pancreas. Cell fractionation into NP-40-soluble and detergent/high salt-insoluble components was performed to assess whether GFAP was located in the cytosolic and/or cytoskeletal compartments of immunoreactive cells. Immunoelectron microscopic analysis was carried out to determine the subcellular distribution of the protein. Peripheral islet cells were stained with anti-GFAP antiserum. These cells were identified as glucagon-secreting cells by immunocytochemical staining of consecutive sections with anti-somatostatin, anti-GFAP, and anti-glucagon antisera. Western blotting analysis of both NP-40-soluble and detergent/high-salt insoluble fractions of isolated islets of Langerhans allowed detection of GFAP in both cytosolic and cytoskeletal compartments. Interestingly, however, the former location was highly predominant. In addition, immunoelectron microscopy localized GFAP associated with the periphery of secretory granules. On the basis of these results, an intriguing role for GFAP in secretory events should be strongly suspected.(J Histochem Cytochem 48:1233-1242, 2000)
 ...
PMID:GFAP is expressed as a major soluble pool associated with glucagon secretory granules in A-cells of mouse pancreas. 1095 Aug 80

Hormonal disorders are the permanent symptoms of renal failure. They concern all known hormones and can be due to quantitative changes of the secretory activity and disturbances of endocrine cell functions. The aim of this study was to establish whether experimental thyroparathyroidectomy in uremic animals causes detectable histomorphological changes in endocrine cells of pancreatic islets. Thyroparathyroidectomy was performed in rats 30 days after nephrectomy. Fragments of pancreatic tissue were collected 14 days after the operation. Paraffin sections were stained with H+E and by silver salt impregnation. Immunohistochemical reactions were conducted using antibodies against calcitoningene-related peptide (CGRP), synaptophysin (SPh), somatostatin (ST), neuron-specific enolase (NSE), and chromogranin (CgA). It was shown that endocrine cells of pancreatic islets in thyroparathyroidectomized rats show intensified immunoreactivity to SPh and ST as compared to the control group of animals. Immunocytochemical reactions for NSE, CgA, and CGRP were negative.
 ...
PMID:Preliminary evaluation of pancreatic islets in rats with experimental uremia and after thyroparathyroidectomy. 1205 34

Postoperative chylous ascites is a rare complication of retroperitoneal surgery. The treatment of postoperative chylous ascites is primarily conservative, consisting of repeated paraceteses, medium chain triglyceride (MCT) diet, salt restriction, diuretics and bowel rest with total parenteral nutrition. Occasionally, chylous ascites may take a protracted course which may necessitate insertion of peritoneo-venous shunts or direct surgical lymphostasis. Recently, Somatostatin was shown to be highly effective in closure of refractory lymphatic fistulas. We present a case of refractory chylous ascites following radical nephrectomy with inferior vena caval thrombectomy that failed to respond to conventional conservative measures and resolved rapidly following the administration of Somatostatin.
 ...
PMID:Chylous ascites after radical nephrectomy and inferior vena cava thrombectomy. Successful conservative management with somatostatin analogue. 1207 12

Eels seem to be a suitable model system for analysing regulatory mechanisms of drinking behavior in vertebrates, since most dipsogens and antidipsogens in mammals influence the drinking rate in the seawater eels similarly. The drinking behavior in fishes consists of swallowing alone, since they live in water and water is constantly held in the mouth for respiration. Therefore, contraction of the upper esophageal sphincter (UES) muscle limits the drinking rate in fishes. The UES of the eel was innervated by the glossopharyngeal-vagal motor complex (GVC) in the medulla oblongata (MO). The GVC neurons were immunoreactive to an antibody raised against choline acetyltransferase (ChAT), an acetylcholine (ACh) synthesizing enzyme, indicating that the eel UES muscle is controlled cholinergically by the GVC. The neuronal activity of the GVC was inhibited by adrenaline or dopamine, suggesting catecholaminergic innervation to the GVC. The AP and the commissural nucleus of Cajal (NCC) in the MO projected to the GVC and were immunoreactive to an antibody raised against tyrosine hydroxylase (TH), rate limiting enzyme to produce catecholamines from tyrosine. Therefore, it is likely that activation in the AP or the NCC may inhibit the GVC and thus relaxes the UES muscle, which allows for water to enter into the esophagus. During passing through the esophagus, the imbibed sea water (SW) was desalted to approximately 1/2 SW, which was further diluted in the stomach and arrived at the intestine as approximately 1/3 SW, almost isotonic to the plasma. Finally, from the diluted SW, the eel intestine absorbed water following the Na(+)-K(+)-2Cl(-) cotransport (NKCC2) system. The NaCl and water absorption across the intestine was regulated by various factors, especially by peptides such as atrial natriuretic peptide (ANP) and somatostatin (SS-25 II). During desalination in the esophagus, however, excess salt enters into the blood circulation, which is liable to raise the plasma osmolarity. However, the eel heart was constricted powerfully by the hyperosmolarity, suggesting that the hyperosmolarity enhances the stroke volume to the gill, where excess salt was extruded powerfully via Na(+)-K(+)-2Cl(-) cotransport (NKCC1) system.
 ...
PMID:Water metabolism in the eel acclimated to sea water: from mouth to intestine. 1466 89


<< Previous 1 2 3 4 5 6 7 Next >>