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)

The effect of potassium on somatostatin secretion from the isolated perfused canine pancreas was studied. Potassium stimulated dose-dependent somatostatin release in a monophasic response pattern. The effect of potassium was abolished in the absence of calcium. Perfusion of 1 micronmol/l atropine and 1 micronmol/l propranolol was without effect on the potassium induced somatostatin release. The results suggest that the stimulatory effect of potassium on somatostatin release is secondary to increases in calcium influx into the D cell. The sympathetic and parasympathetic nerve endings in the pancreas are apparently not involved in the potassium mediated secretory processes.
Scand J Clin Lab Invest 1979 Dec
PMID:Characterization of somatostatin release from the pancreas: the role of potassium. 4 83

Several structures associated with the auditory pathway have been examined by radioimmunoassay for their content of somatostatin. Of these, the medial geniculate body had the highest content, followed by the cochlear nucleus, inferior colliculus, auditory cortex and cochlea. Cochlear perilymph had no detectable somatostatin-like immunoreactivity.
Hear Res 1979 Dec
PMID:Somatostatin along the auditory pathway. 4 84

The perfused stomach in the anaesthetized rat was used to investigate the action of somatostatin on the gastric acid secretion stimulated by gastrin, histamine and carbamylcholine. Evidence is produced that somatostatin competitively inhibits gastrin-stimulated acid secretion whereas it inhibits carbamylcholine-stimulated acid secretion by a mechanism which is non-competitive in nature and it has no action on histamine-stimulated secretion. The model of the persued stomach in the anaesthetized rat seems suitable to study the inhibition caused by drug on stimulated acid secretion.
Agents Actions 1979 Dec
PMID:Utilization of the perfused stomach in anaesthetized rats to study the inhibitory effect of somatostatin in gastric acid secretion. 4 57

The effects of neurotensin on insulin and somatostatin release were examined in isolated pancreatic islets prepared from 3-4 days rats, and maintained in culture for 48 h before use. In the presence of 12 mM glucose, glucagon (50-2,000 ng/ml, i.e. 14-560 nM) caused a 2-fold increase in insulin and somatostatin release. Neurotensin (150 ng/ml, i.e., 100 nM) did not affect the glucagon-stimulated release, nor did it alter the release of either peptide measured at 12 mM glucose in the absence of glucagon. In contrast, neurotension markedly inhibited the release of both insulin and somatostatin that was induced by 23 mM glucose. These observations suggest that neurotensin may modulate the release of insulin and somatostatin evoked by high glucose concentrations, but not that resulting from the action of glucagon on pancreatic islets.
Diabete Metab 1979 Dec
PMID:Neurotensin inhibits glucose but not glucagon-induced insulin and somatostatin release in isolated islets. 4 73

The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphates and potassium were examined in nineteen normal subjects. Plasma phosphorus displayed a highly significant (p less than 0.001) fall with a maximum depression below baseline of 1.11 +/- 0.15 mg/100 ml or 33 +/- 3% (mean +/- SEM); there was a significant correlation (p less than 0.01) between this fall and the insulin peaks induced by arginine. Plasma potassium levels displayed a distinct and significant increase in eleven of the twelve subjects studied; the maximum increase above baseline was 1.02 +/- 0.14 mEq/1 or 27 +/- 4.5% (p less than 0.001). No change occurred in blood pH values determined in four subjects. In six normal subjects, the test was repeated with the addition of somatostatin (250 micrograms bolus, followed by 500 micrograms/hr), which abolished the insulin and growth hormone response to arginine. It also abolished the fall in plasma phosphorus but appeared (if anything) to augment the increase in potassium. These findings show that arginine is responsible for a fall in plasma phosphorus related to the insulin response, and for an increase in plasma potassium of clinical significance, the mechanism(s) of which, however, are still obscure.
Diabete Metab 1979 Dec
PMID:Arginine-induced hypophosphatemia and hyperkaliemia in man. 4 74

Immunocytochemical examination of the islets of Langerhans in various animal species, including man, indicates that insulin-producing cells (B cells), glucagon-producing cells (A cells), and cells producing somatostatin or a somatostatin-like peptide (D cells) are not randomly arranged within the islet. Whenever A cells are found in the islet--i.e., mostly in its peripheral part--they are accompanied by D cells. However, most B cells, which occupy a central position, are in contact only with other B cells. In view of the inhibitory effect of somatostatin on both insulin and glucagon secretion, it is suggested that the arrangement of A, B and D cells is important to the normal and pathological functioning of the islet.
Lancet 1975 Dec 20
PMID:Functional subdivision of islets of Langerhans and possible role of D cells. 5 29

Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. Somatostatin reduced blood-xylose levels by 50-90% after ingestion of this pentose and delayed the peak increment in blood-xylose by 1-2 h. Similar effects on blood-xylose levels and a 30% reduction in splanchnic blood-flow were observed in normal subjects during infusion of somatostatin. Glucagon administration (3 ng per kg per min) or intraduodenal administration of xylose did not reverse somatostatin's effect on xylose tolerance. Somatostatin reduces postprandial hyperglycaemia in diabetes primarily by decreasing and/or delaying carbohydrate absorption rather than enhancing carbohydrate disposal. This effect may be mediated, in part, but a reduction in splanchnic blood-flow. These findings indicate that postprandial hyperglycaemia in diabetes is due primarily to insulin deficiency rather than glucagon excess.
Lancet 1976 Dec 04
PMID:Influence of somatostatin on carbohydrate disposal and absorption in diabetes mellitus. 6 40

Insulin-, glucagon-, and somatostatin-containing cells were evaluated by morphometry in sections of pancreas treated for immunofluorescence. Glucagon- and somatostatin-containing cells were found to be increased in islets of streptozotocin-diabetic rats as compared to control islets.
C R Acad Hebd Seances Acad Sci D 1975 Dec 15
PMID:[Activity of somatostatin-containing cells of the Ilets of Langerhans in experimental diabetes]. 13 Sep 91

Oral glucose tolerance tests (OGTT) were performed for two subsequent days in 4 patients with active acromegaly, 2 patients with prolactin-producing pituitary adenomas and one insulinoma patient. Thirty minutes before the second OGTT 250 mug of somatostatin were injected intravenously as a bolus followed by a somatostatin infusion (500 mug) over 21/2 hours. The OGTTs were pathologic due to the hGH- and hPRL-induced insulin antagonism; they could not be normalized or improved by somatostatin. Only the peak of the blood sugar curve was shifted from one to two and a half hours after glucose administration; insulin and hGH levels were regularly suppressed after somatostatin whereas hPRL remained unchanged in most instances. Gastrin levels increased in all patients during the OGTT, the increase was suppressed in 4 patients. These findings show that the pathologic glucose tolerance due to insulin antagonism could not be improved by somatostatin in contrast to the deteriorated glucose tolerance in insulinopenic states.
Klin Wochenschr 1975 Dec 15
PMID:[Influence of somatastatin on oral glucose tolerance in autonomous hypersecretion of growth hormone, prolactin or insulin (author's transl)]. 17 8

Cells were dispersed from bovine anterior pituitary glands, by digestion with collagenase, and cultured. After 4 days the cell monolayers were incubated with fresh medium containing synthetic hypophysiotropic peptides for 2, 6, or 20 h, and hormone released into the medium was estimated by radioimmunoassay. After 2 h, thyroid releasing hormone (TRH) stimulated the release of thyroid-stimulating hormone (TSH) up to eightfold, and of prolactin (PRL) and follicle-stimulating hormone (FSH) about twofold at a minimal effective concentration of 1 ng/ml; enhanced growth hormone (GH) release was not apparent until 20 h, and release of luteinizing hormone (LH) and adrenocorticotrophic hormone (ACTH) was unaffected. Luteinizing hormone releasing hormone (LH-RH) enhanced release of LH maximally (three- to fourfold) during a 2 h incubation and was effective at 0.1 ng/ml; FSH release was significantly enhanced by about 50% above control level. Growth hormone release inhibiting hormone (GH-RIH)(somatostatin) showed significant effects only in the 20 h incubation; GH release was inhibited by 50% and release of PRL was slightly, but significantly, enhanced. Pituitary cell monolayers apparently permit maximal expression of releasing activities inherent in the hypothalamic hormones.
Can J Physiol Pharmacol 1975 Dec
PMID:Monolayer cultures of dispersed cells from bovine anterior pituitary: responses to synthetic hypophysiotropic peptides. 17 59


1 2 3 4 5 6 7 8 9 10 Next >>