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

The effect of total parenteral nutrition (TPN) in rats on a number of enteroendocrine cells was investigated. The rats were given a continuous intravenous infusion of basal TPN solution for 7 days. Samples from duodenum, jejunum and ileum were collected, immunostained and the immunoreactive cells quantified using a computerised morphometrics system. The endocrine cells containing somatostatin, cholecystokinin (CCK), gastric inhibitory polypeptide (GIP), neurotensin and enteroglucagon were investigated. The results demonstrated a significant reduction in the number of CCK cells in the duodenum and jejunum. In the ileum the neurotensin-immunoreactive cells were significantly increased in number (P less than 0.02). No change was seen in the number of cells immunostained for somatostatin, GIP or enteroglucagon. These data indicate that short term TPN has a definite effect on the enteroendocrine cell population which may be linked to the side effects of TPN seen in man.
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PMID:The effect of total parenteral nutrition in the rat on a sub-group of enteroendocrine cells. 286 21

In six healthy volunteers there were no significant changes during a 300-min control period, whereas gastric inhibitory polypeptide in pharmacological doses first caused a transient and non-significant decrease and then a significant increase in the serum cationic trypsin-like immunoreactivity (CTLI). In another two groups of six healthy subjects, pharmacological doses of cholecystokinin elicited a non-significant increase, whereas somatostatin in pharmacological doses first caused a significant decrease and then a rebound effect with significantly higher levels of serum CTLI.
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PMID:Pharmacological effects of gastric inhibitory polypeptide, cholecystokinin, and somatostatin on the serum levels of cationic trypsin-like immunoreactivity in man. 286 38

Segi's cap, a large aggregation of endocrine cells on the top of intestinal villi, was studied in porcine fetuses and neonates by histological and immunohistochemical methods. The following observations were made: 1) Segi's caps were found in the proximal small intestine in all fetuses larger than 17 cm (beyond 10 weeks of gestation), in neonates before suckling and in 1-4 day-old piglets (suckling neonates); they were not found in a 1 week-old animal. 2) Segi's caps were seen more frequently in the distal duodenum and proximal jejunum than in the proximal and middle duodenum. 3) The Segi's cap consisted mainly of numerous argyrophil cells as demonstrated by Grimelius' method and a few argentaffin cells as identified by a modified Masson-Hamperl's method. 4) Immunohistochemically, ten kinds of immunoreactive cells were dispersed in the mucosal epithelium, outside of Segi's caps, in the proximal small intestine of fetuses: 5-hydroxytryptamine (5-HT)-, gastrin-, bovine pancreatic polypeptide (BPP)-, secretin-, somatostatin-, cholecystokinin-, gastric inhibitory polypeptide (GIP)-, motilin-, leucine-enkephalin- and neurotensin-immunoreactive cells. Except for neurotensin-immunoreactive cells, all of these cells were detected also in the caps. 5) Regional differences were noted in the distribution of cells in the caps; gastrin-, BPP- and secretin-immunoreactive cells were dominant in the caps in the proximal duodenum, while 5-HT-immunoreactive cells were most numerous in those in the proximal jejunum.
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PMID:Histological and immunohistochemical studies of the Segi's cap, a large aggregation of endocrine cells on the intestinal villi of porcine fetuses and neonates. 286 50

The postprandial release of immunoreactive insulin, glucagon, gastrin, somatostatin, pancreatic polypeptide (PP), and gastric inhibitory polypeptide (GIP) was studied in parallel with the absorption of sugars and amino acids in conscious pigs. Six pigs fitted with permanent catheters in the portal vein and arterial blood system as well as within an electromagnetic flow probe around the portal vein received successively at 3-day intervals, three meals of 800 g each containing 0, 14, or 28% protein (semisynthetic diets based on fish protein). Blood samples were collected and portal blood flow was recorded during a postprandial period of 8 h. For the same level of feed intake, an increase in the dietary protein concentration led to a higher alpha-amino nitrogen absorption and to a lower appearance of reducing sugars in the portal vein; in addition, the carbohydrate absorption efficiency (amounts absorbed as a percentage of amounts ingested) was reduced, showing the competition between the absorption of amino acids and glucose. The largest absorption occurred during the first 4 h after the meal, but neither the digestion of proteins nor that of carbohydrates were finished 8 h after the meal since portoarterial differences could still be observed. All test meals induced a rise of portal and peripheral concentrations of insulin, gastrin, somatostatin, and PP, and of the systemic level of GIP. Glucagon increased after the 28% protein meal only. The rise of plasma insulin paralleled that of blood glucose, and bore a significant positive relationship to the systemic GIP level in the early postprandial period. In terms of absolute amounts, portoarterial concentration gradients increased postprandially. Insulin release was significantly the highest after intake of the 14% protein diet. The gastrin response was significantly correlated to the amount of protein. Similarly the release of glucagon and somatostatin tended to increase with increasing dietary amount, but differences failed to reach significance (P less than 0.05), except for glucagon 2 h after the meal. There were very close relationships between the hourly amounts of alpha-amino nitrogen absorbed and gastrin and glucagon production, as between insulin and PP secretions. From the present results, the induction of physiological increments of plasma peptide concentration in 60-kg pigs would require infusion rates of about 50-250 micrograms/h for insulin, 1-4 micrograms/h for gastrin 17, 5-10 micrograms/h for glucagon and somatostatin, and 5-50 micrograms/h for PP.
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PMID:Metabolic and hormonal effects of test meals with various protein contents in pigs. 286 30

In six healthy persons receiving graded intravenous infusions of synthetic somatostatin the plasma motilin concentrations decreased significantly (p less than 0.05) already with doses giving physiological plasma somatostatin levels, and a rebound of plasma motilin was observed after cessation of infusion of pharmacological somatostatin doses. After an intravenous secretin infusion (280 pmol/kg-h) producing pharmacological plasma secretin concentrations, a comparable plasma somatostatin increase was observed together with a substantial decrease in plasma motilin (p less than 0.05). Infusion of cholecystokinin in a pharmacological dose and of gastric inhibitory polypeptide (GIP) in doses giving plasma GIP levels in the physiological range had no effect on plasma somatostatin or motilin. Circulating plasma somatostatin may be a physiological modulator of the motilin release, and the plasma motilin fall seen during infusion of pharmacological doses of secretin may possibly be explained by the secretin-induced somatostatin release occurring simultaneously.
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PMID:Evidence of somatostatin as a humoral modulator of motilin release in man. A study of plasma motilin and somatostatin during intravenous infusion of somatostatin, secretin, cholecystokinin, and gastric inhibitory polypeptide. 287 17

The present study in the rat demonstrates an inhibitory mechanism of gastric emptying, sensitive to the osmolality of a liquid meal. Gastric emptying and intestinal transit were studied in groups that differed with regard to the osmolality of the gastric or duodenal instillation, experimental time, and indomethacin treatment. By intragastric instillation animals were fed an aqueous solution containing the nonabsorbable marker 51CrO2-4. After certain fixed time intervals the rats were killed and the stomach and small intestine were dissected out en bloc. The distribution of the isotope along the gastrointestinal canal was then determined. Intestinal transit was evaluated in a similar manner. The marker solution was introduced into the duodenum. A hyperosmolar solution, 1200 mOsm kg-1, was emptied from the stomach significantly more slowly than was an iso-osmolar solution, 300 mOsm kg-1. Of the iso- and hyper-osmolar solutions 87% and 74%, respectively, were emptied in 1 h. The isotope distribution along the intestinal canal after intraduodenal instillation was not affected by the osmolality of the installation. The osmotic inhibition of gastric emptying was not affected by indomethacin treatment (4 mg kg-1) or related to elevated plasma levels of gastrin, neurotensin, somatostatin, or gastric inhibitory polypeptide.
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PMID:Gastric emptying and intestinal transit of hyperosmolar solutions in relation to indomethacin and certain gut polypeptides in the rat. 287 19

The effects of various biologically active peptides on net jejunal water and electrolyte fluxes were studied in dogs in vivo. Vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP), glucagon, gastrin, bombesin and neurotensin all had secretagogue activity, while methionine enkephalin stimulated net absorption. Somatostatin had no effect on net basal water and electrolyte transport, but inhibited glucagon-stimulated secretion. Secretin, calcitonin, substance P and pancreatic polypeptide (PP) did not have any effect on net water and electrolyte transport in the doses used in these experiments. The precise role played by these peptides in the control of intestinal transport has still to be determined. Studies in man have confirmed that food in the proximal small bowel stimulates secretion at sites remote from the application of food, and abnormal secretion of some peptides (e.g. VIP) has been associated with diarrhoea. Somatostatin has been used successfully to reduce the volume of certain types of secretory diarrhoea. Methods used in these experiments have been applied to the study of the composition and absorption characteristics of solutions used for oral rehydration in diarrhoea and in exercise-induced dehydration. Glucose polymers have been shown to be absorbed as rapidly as glucose from the jejunum.
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PMID:The effect of luminal and hormonal factors on small intestinal water and electrolyte transport. 287 15

The effects of a somatostatin analogue, SMS 201-995, and somatostatin-14 on gastrin and insulin release from the isolated perfused rat stomach and pancreas were studied. Equipotent effects were observed on the inhibition of basal gastrin release from the stomach. SMS 201-995 was approximately 14 times less effective than somatostatin-14 (molar basis) in the pancreas. At a high glucose concentration (17.6 mM), neither the analogue nor the peptide inhibited insulin release, but at a glucose concentration of 8.8 mM, there was significant inhibition. In the presence of 10 mM arginine plus glucose at a concentration of either 8.8 or 17.6 mM, insulin secretion was reduced by both SMS 201-995 and somatostatin-14 to levels obtained with glucose alone. However, when gastric inhibitory polypeptide (10 ng/ml) in the presence of 8.8 mM glucose was used to stimulate insulin release, somatostatin-14 completely inhibited the insulinotropic action of gastric inhibitory polypeptide while SMS 201-995 was without effect. Studies with this analogue suggest that arginine and gastric inhibitory polypeptide stimulate insulin release via different mechanisms.
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PMID:Comparison of the effect of somatostatin and an analogue, SMS 201-995, on gastrin and insulin secretion from isolated perfused rat stomach and pancreas. 287 49

Elevated serum levels of gastrin, pancreatic polypeptide, and glucagon were found in 10 uraemic patients, whereas gastric inhibitory polypeptide and somatostatin levels were normal. After renal transplantation there was a significant reduction in serum gastrin (median, 5 pmol/l; p = 0.05, n = 9), pancreatic polypeptide (145 pmol/l; p less than 0.01, n = 9), GIP (9.5 pmol/l; p = 0.02, n = 7), and glucagon (92 pg/l; p less than 0.02, n = 9), whereas no alteration was seen in the somatostatin level. Meal stimulation produced consistent increases in serum levels of all hormones, and the response appeared to be unchanged after renal transplantation.
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PMID:The immediate effect of human renal transplantation on basal and meal-stimulated levels of gastrointestinal hormones. 288 97

We investigated the impact of blood glucose normalization on plasma levels of somatostatin-like immunoreactivity (SLI) in subjects with C-peptide-negative insulin-dependent diabetes mellitus (IDDM) and in totally pancreatectomized patients. Patients were studied during hyperglycemia and during normoglycemia, which was attained by Biostator-directed feedback insulin infusion. The experiments were performed in the fasted state and after a standardized breakfast. In IDDM (n = 6), basal levels of SLI were significantly higher than in nondiabetic subjects (n = 18). In IDDM, normalization of hyperglycemia was followed by a 40% decline in basal SLI (P less than .05). After the meal, SLI increased to the same absolute levels with or without feedback insulin treatment; however, the incremental response was 60% higher during feedback insulin treatment (P less than .05). Treatment also suppressed fasting and postprandial levels of glucagon, whereas gastric inhibitory polypeptide (GIP) levels were unaltered. In four pancreatectomized patients, normoglycemia tended to lower plasma levels of SLI by 50% (P less than .1). After breakfast, an SLI response was noted during normoglycemia, whereas no significant effect of the meal was seen during hyperglycemia. We conclude that in IDDM and in totally pancreatectomized patients, administration of insulin with subsequent normalization of blood glucose is accompanied by a decline in plasma levels of SLI in the fasted state, whereas the apparent response to a meal is enhanced. These effects on plasma levels of SLI probably reflect to a major extent release of somatostatin from the gastrointestinal tract.
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PMID:Basal and meal-induced somatostatin-like immunoreactivity in healthy subjects and in IDDM and totally pancreatectomized patients. Effects of acute blood glucose normalization. 288 57


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