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)

Immunocytochemistry (ICC) and a reverse hemolytic plaque assay for GH were used to investigate the temporal relationships between the initiation of hormone storage and release by developing somatotropes and the onset of responsiveness of these cells to stimulatory and inhibitory secretagogues. Anterior pituitaries obtained from rats on days 18-21 of fetal development (pups were generally delivered on fetal day 22, which is equivalent to day 0 of neonatal life) were monodispersed with trypsin, cultured for 24 h, and then subjected to reverse hemolytic plaque assay and/or ICC for GH. GH-containing cells (determined by ICC) were extremely rare (less than 1%) in cultures derived from day 18 fetuses, but accounted for 22.4%, 25.2%, and 24.5% of all cells in cultures from day 19-21 fetuses, respectively. The proportion of GH-releasing cells, as determined in a long term (120-min incubation with antibody) plaque assay, was less than 1%, 22.4%, and 22.9% for days 18, 20, and 21, respectively, but only 13.6% for day 19 cells. Thus, many pituitary cells from day 19 fetuses contained, but did not release, GH. While GH-releasing factor (1-44) (1 X 10(-7) M) had no effect on the percentage of GH plaque-forming cells in long term incubations, it enhanced (by approximately the same degree in day 19-21 groups) the percentage of cells that formed plaques and the size of the plaques in short term (45-min) incubations with antibody. Somatostatin (1 X 10(-7) M) exerted inhibitory effects on these variables when tested in long term incubations, and age of the donor rats did not influence pituitary responsiveness to this secretagogue. These results suggest that the capacities of fetal somatotropes to store GH and release it under basal and regulated conditions are attained, in large part, within an extremely narrow time frame between days 18 and 19 of fetal development.
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PMID:Functional maturation of somatotropes in fetal rat pituitaries: analysis by reverse hemolytic plaque assay. 285 84

The effect of three concentrations of high-methoxy apple pectin (5, 10, and 15 g), on solid-liquid meal digestion was studied in 12 healthy men by the gastrointestinal intubation technique. The gastric emptying of water and carbohydrates is significantly reduced only after 10 and 15 g pectin. The changes in gastric pH are similar for pectin-free and pectin-containing meals. Cumulative lipase and trypsin outputs are not significantly different with and without pectin. When gastric uronic acid concentration is above 6 g/l, the duodenal absorption of carbohydrates is significantly reduced (p less than 0.001). The mean blood glucose levels with 10 and 15 g pectin are significantly higher than the control values at 180 min (p less than 0.05). Pectin does not modify serum concentrations of secretin, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), and somatostatin but serum motilin and gastrin levels are below the control values after high fiber meal.
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PMID:Effect of increased amounts of pectin on a solid-liquid meal digestion in healthy man. 286 75

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

We have evaluated the role of cellular Ca2+ transport associated with stimulus-secretion coupling in prolactin (PRL) producing rat pituitary adenoma cells (GH3 cells). The action of different substances, known to modify PRL secretion, on release of 45Ca2+ from preloaded cells were examined. Surface-bound 45Ca2+ was removed by pretreatment with trypsin in EDTA buffer. During the first 6 min, basal efflux of 45Ca2+ occurred at a constant rate (0.24 min-1) at 37 degrees C. Addition of TRH (5 X 10(-7) M) resulted in an immediate enhancement of 45Ca2+ release representing about 20% of the remaining cellular 45Ca2+. In the same experiments PRL secretion increased by 45%. The EDTA in the external medium reduced the basal rate of 45Ca2+ release by 60%, but did not apparently affect the TRH-stimulated release. Somatostatin (10(-6) M) and verapamil (5 X 10(-5) M) inhibited both basal and TRH-stimulated PRL secretion, whereas high extracellular concentration of K+ (5 X 10(-2) M) had a stimulatory effect. However, neither of these treatments changed cellular 45Ca2+ release. Interference with energy-dependent Ca2+ transport by using metabolic inhibitors (iodoacetate, 6 X 10(-3) M; and antimycin, 2 X 10(-6) M) or by replacing Na+ in the medium by choline or by lowering the incubation temperature from 37 to 25 degrees C, had no effect on TRH-stimulated 45Ca2+ release although basal and TRH-stimulated PRL secretion were reduced. Thus, TRH apparently releases 45Ca2+ from calcium binding sites in the cell membrane.
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PMID:On the functional relationship between 45Ca2+ release and prolactin secretion in cultured rat pituitary tumour (GH3) cells. 287 12

The neurotransmitter of the non-adrenergic non-cholinergic inhibitory innervation of the stomach is still unknown. We studied the effect of a series of neurotransmitter candidates, ATP, [Leu]enkephalin and [Met]enkephalin, somatostatin, neurotensin and VIP, in the rat gastric fundus and compared these effects with the response to electrical stimulation of the non-adrenergic non-cholinergic inhibitory neurons. Rats of both sexes were treated with reserpine (5 mg . kg-1 intraperitoneally) 24 h before killing. Longitudinal muscle strips of the gastric fundus were prepared and mounted between parallel platinum electrodes in Krebs solution containing atropine 10(-6) M and serotonin 3.10(-6) M. A maximal relaxatory response was obtained on transmural stimulation of the strips at supramaximal voltage, 1 msec and 5 Hz. ATP (10(-6)-10(-3) M) elicited a biphasic response, a small relaxation followed by a contraction. The maximal relaxatory response induced by ATP was much lower than that induced by transmural stimulation during 45 sec (37.3% versus 166.2%, where 100% is the maximal contractile response to ATP, n = 17). Desensitization to ATP did not influence the relaxation induced by transmural stimulation. [Met]enkephalin, [Leu]enkephalin and naloxone did not change the tone of the strips or the amplitude of the electrically induced relaxation. Somatostatin had no influence while neurotensin induced a concentration-dependent contraction from 10(-9) M or 10(-8) M on. VIP (10(-10)-3.10(-8) M) induced a concentration-dependent relaxation. The maximal relaxation induced by VIP was 120.8% of that induced by transmural stimulation (n = 16). The relaxation induced by VIP 10(-8) M, left in contact with the tissue for 10 min, was comparable to that induced by transmural stimulation during 10 min, except for a lag time of more than 10 sec after the addition of VIP. The relaxation induced by VIP was not influenced by tetrodotoxin, phentolamine or propranolol. The peptidase trypsin (10(-6) M) antagonized the relaxation by exogenously added VIP but did not influence the electrically induced relaxation. The results obtained in this study show that, of the substances tested, only VIP mimics the relaxation induced by stimulation of the inhibitory non-adrenergic non-cholinergic neurons in the rat gastric fundus; VIP therefore seems a reasonable candidate as neurotransmitter of these neurons.
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PMID:Study on the possible neurotransmitter of the non-adrenergic non-cholinergic innervation of the rat gastric fundus. 287

The arachidonate cascade of human or rat platelets were found to be modified by peptides (bradykinin, angiotensin I, angiotensin II, Asp1-Val5-angiotensin II-amide, somatostatin) and proteases (trypsin, kallikrein). The lipoxygenase pathway was not altered by angiotensin I, angiotensin II, trypsin and kallikrein, while the synthesis some of the cyclooxygenase products was selectively changed by these substances. Bradykinin and somatostatin resulted in an attenuated formation of 12-HPETE and 12-HETE - U shape dose response curve, at the same time the synthesis of cyclooxygenase metabolites was increased - bell shape dose response curve. Asp1-Val5-angiotensin II-amide increased the synthesis of lipoxygenase products and diminished the formation of TxB2. At the same time this peptide selectively induced the enzymatic release of PGD2 from platelets. These peptides and proteolytic enzymes might have physiologic significance in the "Ying-Yang" balance in one hand between lipoxygenase and cyclooxygenase metabolites and on the other between the proaggregatory and antiaggregatory substances released from platelets.
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PMID:The action of peptides and proteases on the arachidonate cascade of human and rat platelets. 288 Apr 82

The effect of the long-acting somatostatin analogue Sandostatin (SMS 201-995) on intestinal absorption and propagation (mouth-to-caecum transit time; MCTT), on pancreatic secretion and on gall bladder contraction after direct (secretin-pancreozymin test) and indirect stimulation (Lundh meal), and on meal-induced responses of seven gastrointestinal regulatory peptides has been investigated. In a double-blind cross-over study, 9 healthy volunteers completed two 7-day periods with subcutaneous injections of either placebo or 25 micrograms SMS 201-995 twice daily. Mean faecal fat excretion was increased to 19.2 g/day and MCTT was three times longer during the SMS period. After duodenal infusion of a mixture containing D-galactose, D-xylose and triglycerides, SMS 201-995 significantly reduced the serum concentrations of D-galactose but increased serum levels of D-xylose. After 6 days of pretreatment, SMS 201-995 completely suppressed duodenal trypsin, lipase and bilirubin increases in response to endogenous stimulation by a Lundh meal. Concomitantly, cholecystokinin (CCK) release and gall bladder contraction were almost abolished. Compared with placebo, SMS 201-995 significantly diminished pancreatic amylase, trypsin and lipase output after stimulation with CCK, while the secretion of fluid and bicarbonate in response to secretin was unchanged. This inhibition of enzyme response was significantly more marked after a single injection of the analogue than after pretreatment for 7 days and did not reach the level of exocrine pancreatic insufficiency. CCK-induced gall bladder contraction was significantly inhibited by a single dose of 25 micrograms SMS 201-995 but not after 7 days of pretreatment with the somatostatin analogue.
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PMID:Effect of the somatostatin analogue sandostatin (SMS 201-995) on gastrointestinal, pancreatic and biliary function and hormone release in normal men. 288 60

This study was undertaken to determine the effect of atropine and somatostatin, two inhibitors of intraduodenal pancreatic enzyme secretion, on bombesin-stimulated release of plasma immunoreactive trypsin in 6 healthy volunteers. Infusion of 5 ng/kg.min bombesin during 30 min induced significant increases in plasma trypsin from 206 +/- 20 to 334 +/- 44 ng/ml (p less than 0.01). Atropine (15 ng/kg as i.v. bolus followed by 5 ng/kg.h) had no influence on the bombesin-stimulated increase in plasma immunoreactive trypsin (207 +/- 20 to 326 +/- 54 ng/ml). Somatostatin (125 micrograms as i.v. bolus followed by 125 micrograms/h) also failed to inhibit the plasma trypsin response to bombesin (207 +/- 18 to 663 +/- 166 ng/ml). These results point to major differences in the regulation of plasma and intraduodenal trypsin secretion.
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PMID:Effect of atropine and somatostatin on bombesin-stimulated plasma immunoreactive trypsin release in man. 288 97

A 60 year old man developed steatorrhoea, weight loss, mild diabetes mellitus, labile hypertension and limb cramps. Raised plasma concentrations of catecholamines, particularly noradrenaline and a computed tomography-scan showing an adrenal tumour strongly suggested a pheochromocytoma. Adrenoreceptor blockade reversed the symptoms, decreased faecal fat, and increased duodenal trypsin to normal concentrations. After adrenalectomy the patient was asymptomatic and there was no steatorrhoea. The blood glucose concentrations became normal. Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin.
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PMID:A mixed endocrine adrenal tumour causing steatorrhoea. 289 May 60

The aim of this study was to determine the effect of wheat bran consumption on exocrine pancreas secretion in pigs. Sixteen Large-White pigs were divided into two groups. The first group (control) was fed a diet without wheat bran and the second one (experimental) a diet containing 40% wheat bran. After one week the animals were fitted with two permanent fistulae (in the pancreatic duct and the duodenum) and/or with a catheter in a carotid artery. After an 8-day recovery period, pancreatic secretion (volume, protein content and output, chymotrypsin, trypsin, lipase and amylase activities) and plasma levels of some gastro-intestinal peptides [secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP), somatostatin and pancreatic polypeptide (PP)] were measured over an experimental period of 5 days. The results show that wheat bran intake induced an increase in the volume (+ 115%) and protein output (+ 36%) of the pancreatic juice secreted in a 24-hour period, whereas protein concentration decreased. All enzyme activities were enhanced by wheat bran. The plasma levels of secretin, VIP, somatostatin and PP were higher in the experimental than in the control group. On the contrary, plasma CCK levels were not affected by wheat bran consumption.
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PMID:Effects of wheat bran on exocrine pancreas secretion in the pig. 289 Nov 62


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