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 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.
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PMID:Arginine-induced hypophosphatemia and hyperkaliemia in man. 4 74

The renal effect of cyclic somatostatin was studied on healthy subjects. The somatostatin was used at therapeutical dose in intravenous infusion. Somatostatin decreases the renal plasma flow, glomerular filtration rate, osmotic and free water clearances, sodium and potassium excretion and the tubular reabsorption of phosphorus while urinary osmolality increases. Under somatostatin infusion the urinary excretion of catecholamines, PGE2, PGF2 alfa and the plasma renin activity and the plasma concentration of glucagon and growth hormone decrease. The antidiuretic activity of somatostatin is due to a) a direct haemodinamic effect, b) an influence on the renal tubular transport as well and also c) because of change the water handling in the collecting ducts.
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PMID:[Effect of somatostatin on kidney function]. 168 89

The cyclic peptide SMS 201-995 (+)D-Phe1-Cys2-Phe3-D-Trp4-(+)Lys5-Thr6-++ +Cys7-Thr(ol)8 is an analog of somatostatin and binds to lipid membranes by an electrostatic/hydrophobic mechanism. The structural changes accompanying the binding process were investigated with circular dichroism (CD), fluorescence spectroscopy, and phosphorus and deuterium nuclear magnetic resonance. The peptide penetrates into the lipid bilayer and the binding is accompanied by a small change in the CD spectrum suggesting the formation of beta-ordered structures. The fluorescence emission spectrum of the tryptophan side chain exhibits a blue shift and an intensity enhancement of the emission maximum, providing evidence that this residue is located in the inner part of the phospholipid headgroup region with a dielectric constant of epsilon approximately 7. The peptide diffuses rapidly in the plane of the membrane, changing the lipid headgroup conformation. This was demonstrated by selectively deuterating the two choline segments and measuring the deuterium spectra as a function of the bound peptide concentrations. A linear variation of the quadrupole splitting with the mol fraction of bound peptide was observed. The molecular origin of this effect is a distinct change in the orientation of the phosphocholine dipole, moving the N+ end of the dipole away from the membrane surface into the water phase. This type of headgroup rotation appears to be the general response of the zwitterionic phosphocholine headgroup to cationic surface charges. However, peptides appear to be the most efficient modulators of the lipid headgroup structure known to date.
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PMID:Peptide binding to lipid membranes. Spectroscopic studies on the insertion of a cyclic somatostatin analog into phospholipid bilayers. 199 58

The effect of somatostatin-14 on gastric emptying, as well as on serum concentrations of gastrin, insulin, glucose, calcium, and phosphorus after ingestion of a mixed solid-liquid meal was examined in seven healthy men in a double-blind placebo-controlled study. An i.v. bolus injection of 61 nmol somatostatin was followed by 244 nmol infused at a constant rate over 90 minutes. Gastric emptying of a radiolabelled meal was surveyed with the use of a gamma camera. A weak delaying effect of somatostatin on gastric emptying of a solid meal did not prove to be statistically significant. Somatostatin decreased significantly the postprandial gastrin release: the area under the gastrin curve, AUC0-90, 9954 +/- 2287 ng.l-1 min (placebo) vs 5327 +/- 718 ng.l-1 min (somatostatin), p less than 0.05. At the same time suppression of the postprandial insulin release by somatostatin was observed--area under the insulin curve, AUC0-90, 1450 +/- 161 mU.l-1 min (placebo) vs 501 +/- 60 mU.l-1 min (somatostatin), p less than 0.002. The postprandial increase in serum glucose concentration was initially attenuated, and shifted towards the end of somatostatin infusion, when referred to the placebo situation. Somatostatin did not change significantly the serum calcium or phosphorus concentrations. The results obtained indicate that somatostatin's effect on gastric evacuation is less pronounced in contrast to the significant inhibitory influence of somatostatin on release of gastrointestinal hormones.
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PMID:Effect of somatostatin-14 on gastric emptying and on gastrin and insulin release after ingestion of a mixed solid-liquid meal in man. 257 74

Plasma somatostatin (SRIF), growth hormone (GH), somatomedin C (IGF1), osteocalcin (BGP), 1,25-dihydroxyvitamin D (1,25-(OH)2D), calcium and inorganic phosphorus were measured in 10 chronically-catheterized fetal calves and in their dams during the two last months of gestation. Thus fetal life is associated with high levels of GH (1.53 +/- 0.14 nmol.l-1), BGP (64 +/- 4 nmol), Ca (2.90 +/- 0.06 nmol.l-1) compared to the results obtained in the pregnant cows. The first week of postnatal life was associated with a tremendous increase in plasma SRIF concentration (from 36 +/- 5 to 106 +/- 15 pmol.l-1; P less than 0.01). These results agree with an intense bone growth during the end of fetal life in the bovine species. However, IG 1 might not play a major role in the regulation of fetal skeletal growth during this period.
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PMID:Systemic bone growth factors concentrations in calves during the perinatal period. 290 75

Fifteen male Holstein X Frisian calves, weighing 65 +/- 3 kg and fed a milk replacer twice daily were fitted with a return cannula loop, chronically implanted at 10 days of age in the pancreatic duct, were used. In six successive experiments we have observed the influence of an intravenous infusion of secretin, cholecystokinin pancreozymin (CCK-PZ), vasoactive intestinal peptide (VIP), glucagon, gastrin and somatostatin on pancreatic juice flow rate, and on the excretion of proteins, calcium, inorganic phosphorus, zinc and amylase activity of pancreatic juice. In two other experiments, we have studied the interaction of secretin (or CCK-PZ) with somatostatin (SRIF). Each experiment was performed 5 h after calves feeding and no milk was given to the animals during the time of sampling. Our results indicate that the endocrine regulation of the exocrine pancreas in young calves is similar to that described in other mammals. Secretin and CCK-PZ increased significantly excretion of water, calcium, magnesium, inorganic phosphorus, zinc, proteins and amylase activity. Somatostatin and glucagon inhibited effects observed with two precedent hormones. Gastrin increased pancreatic juice flow rate but excretion of protein and amylase activity do not varied significantly. VIP showed no significant effect on pancreatic excretion of water, minerals, proteins and amylase activity. However, our animals seem to be characterized by a more intense excretion of proteins and amylase in the pancreatic juice following secretin than after CCK-PZ infusion.
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PMID:The endocrine regulation of exocrine pancreas in preruminant milk-fed calves. 610 15

Eight patients suffering from primary hyperparathyroidism were studied in basal conditions, i.e. during a saline infusion and under somatostatin administration (a 250 micrograms bolus injection followed by continuous infusion of 500 micrograms per hour over 240 min). The calcium metabolism was estimated from (i) concentrations of plasma calcium, phosphorus, 25-hydroxyvitamin D (25-OH-D), iPTH and (ii) intestinal calcium absorption determined by a double radiotracer technique using oral 47Ca and IV 45Ca. The results show that somatostatin produced no significant change in calcium, phosphorus, 25-OH-D or iPTH levels. On the contrary, the fractional absorption of calcium (FA Ca), expressed as a percentage of the total oral dose and measured at 30 minute intervals over 240 min, was significantly depressed with somatostatin during the first 2 hours. Beyond the second hour FA Ca remained slightly depressed with somatostatin, but was not significantly different from the basal conditions. From the present results, we conclude that somatostatin slows down calcium absorption, while the total amount of calcium absorbed at the completion of the absorption process is not significantly diminished. Furthermore, as 25-OH-D and iPTH remained unchanged, somatostatin seems to have no effect on the hormonal control of calcium absorption. Therefore, we suggest that somatostatin has only a mechanical effect on calcium absorption, slowing down the intestinal transit.
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PMID:Effects of somatostatin on intestinal calcium absorption in man with primary hyperparathyroidism. 613 May 77

Following previous work showing that i.v. arginine induces a fall in blood phosphorus and an increase in blood potassium in normal subjects, investigation of the mechanism underlying these metabolic changes was extended to a group of 14 insulin-dependent diabetics and a further 6 normal volunteers. In the diabetics, arginine (0.5 g/kg body weight) in 30 min caused a slight, but significant fall in blood phosphorus (delta = -0.40 +/- 0.04 mg/ml p less than 0.01). This was well below the fall noted in the normal subjects, which, as demonstrated in the earlier study, is to a great extent mediated by insulin. The increase in blood potassium was much more marked than in the normal subjects (delta = + 1.42 +/- 0.15 mEq /l; p less than 0.001) and rose to pathological levels (5.6 to 6.5. mEg/l) in 9 out of 14 patients. There were no significant changes in blood pH, plasma osmolality, or plasma aldosterone. Inhibition of the glucagon response to arginine by means of a priming dose of 250 micrograms somatostatin, followed by infusion of 1,500 micrograms/hr, did not abolish the rise in blood potassium. These findings indicate that insulin protect against arginine-induced hyperkalaemia and that this metabolic alteration does not depend on glucagon, acidosis, enhance plasma osmolality, nor the suppression of aldosterone secretion. Persons with low insulin secretion due, for example, to stress or diabetes, run the risk of pathological hyperkalaemia if subjected to i.v. infusion of arginine.
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PMID:The risk of pronounced hyperkalaemia after arginine infusion in the diabetic subject. 731 14

Although receptors for somatostatin are found in bone cells, the effect of somatostatin analogs on calcium metabolism is unknown. The authors studied, in a metabolic ward, the effect of octreotide (a long-acting somatostatin analog) and a placebo in two 6-day calcium balance periods in 8 children with Duchenne muscular dystrophy. As expected, octreotide (2 micrograms/kg, subcutaneously, every 8 hours) reduced serum growth hormone and somatomedin (IGF-1) to levels found in growth hormone deficiency. Octreotide enhanced calcium retention by 30% (96 mg daily [P < 0.04]) in 7 boys for whom complete data (diet, urine, and fecal calcium) were available. In 6 children with urinary calcium excretion (Uca) greater than 50 mg daily, octreotide markedly lowered Uca, from 114 +/- 23 mg daily to 61 +/- 9 mg daily (P < 0.03). Calcium retention occurred in patients with or without initial hypercalciuria, but the higher the basal Uca, the greater was the inhibition by octreotide (r = 0.79; P < 0.03). Inactive, nonambulatory patients had a more pronounced response of Uca to octreotide (P < 0.02). Octreotide caused a mild, nonsignificant reduction in fecal calcium, with no major changes in serum calcium, phosphorus, parathyroid hormone, urinary excretion of sodium and potassium, or in creatinine clearance. Based on the current observations and the presence of receptors for somatostatin in bone cells, this hormone may have, at least on a short-term basis, an anabolic effect on calcium, perhaps favoring its deposition in bone.
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PMID:Octreotide enhances positive calcium balance in Duchenne muscular dystrophy. 766 11

Parathyroid carcinoma (PC) is a rare endocrine tumor whose management is difficult whenever surgery does not achieve complete en bloc resection or recurrence is detected. Medical options (mainly bisphosphonates) are scanty and often associated with toxic side-effects. We present a case report of a patient with recurrent PC after two surgical interventions who was treated with octreotide (SMS-201) taken into account the positive somatostatin staining of the specimen obtained during the last surgery. Short term effects (-2 weeks-) included a decrease in urinary calcium excretion paired with a simultaneous increase in urinary phosphorus excretion. Later on, continuous subcutaneous octreotide administration kept urinary calcium excretion at low levels and this effect was completely reversible/reinducible upon discontinuation/reintroduction of the drug. Neither iPTH nor total serum calcium were modified at short or long term basis. The lack of clear-cut therapeutic effects make this findings a pure clinical observation. Thus, octreotide cannot be recommended for the treatment of parathyroid carcinoma.
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PMID:[Effects of octreotide on serum and urine electrolytes in a patient with parathyroid carcinoma: clinical case]. 1181 19


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