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)

Four weeks after 70% resection of the pancreas in the rat, serum levels of calcium, inorganic phosphate, magnesium, parathyroid hormone and calcitonin, as well as femur dry weight, volume, mean specific density, and mineral content were investigated. The urinary excretion of cAMP and hydroxyproline was measured. Additionally, residual pancreatic amylase content, fasting blood levels of insulin, glucagon, somatostatin and glucose were determined, and the mineral balance (calcium, phosphate) studied. Residual pancreatic amylase content was decreased to 22% of control values, fasting serum glucose and plasma glucagon were increased. Fecal excretion of calcium and phosphate was unchanged, but their balance was increased. Serum calcitonin and the mean specific density of femurs were decreased. All the other variables were unchanged. We conclude that in the rat, 70% pancreatic resection 1) probably does not have any harmful effects on calcium metabolism and bone mineralization in the short term postoperatively, 2) provokes mild hyperglucagonemia, the molecular nature and the origin of which need further elucidation.
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PMID:Influence of 70 percent pancreatic resection on serum and bone calcium in the rat--a preliminary report. 342 61

Effects of somatostatin on basal and low calcium-, isoproterenol- or dibutryl cyclic AMP (DBcAMP)-stimulated parathyroid hormone (PTH) secretion were evaluated in vitro with bovine parathyroid tissue. Low calcium, isoproterenol or DBcAMP alone significantly stimulated PTH secretion. Somatostatin 1 or 4 microgram/ml significantly inhibited these stimulated PTH secretions. Inhibition of isoproterenol-stimulated PTH secretion was more complete than was the inhibition of low calcium- or DBcAMP-stimulated secretion. The studies indicate that somatostatin inhibits PTH secretion by an action distal to cAMP generation. The more complete inhibition of isoproterenol-stimulated PTH secretion suggests that somatostatin may also have additional effects on or proximal to the formation of cyclic AMP.
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PMID:Mode of action of somatostatin in inhibiting parathyroid hormone secretion. 610 93

The release of immunoreactive gastrin and somatostatin form the gastric antrum was studied in anesthetized pigs after parathyroid hormone (PTH) infusion into the antral circulation. PTH (40 units/20 min) was infused into the right gastro-epiploic artery. Blood was sampled from the right gastro-epiploic vein (antral venous blood) and from the superior vena cava (mixed venous blood). The basal gastrin concentration in antral venous blood was 17 times higher than that in mixed venous blood (1220 + 367 versus 71 +25 pmol/1, mean +SE). The somatostatin concentrations in antral and mixed venous blood were 127 +20 and 82 +23 pg/ml (mean +SE), respectively. After PTH infusion the gastrin level both in antral and mixed venous blood increased significantly without inducing systemic hypercalcemia. PTH infusion did not significantly influence the somatostatin level either in antral venous blood or in mixed venous blood. The findings demonstrate that PTH can induce gastrin release from the gastric antrum without concomitant systemic hypercalcemia and that this release of gastrin is not accompanied by a change in the somatostatin level in antral venous blood.
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PMID:Effect of parathyroid hormone on gastrin and somatostatin release from the gastric antrum. 611 27

Experiments were designed to study the effect of exogenous somatostatin (S) on basal levels or parathyroid hormone (PTH) and on PTH responses to isoproterenol (ISO), adrenaline (A) or ethyleneglycol-bis (beta-aminoethylether) N,N'-tetraacetate (EGTA) in cattle. During S infusions (6.11 nmol injected iv as a bolus and 0.82 nmol/kg/min infused iv for 30 or 60 min) plasma levels of PTH and calcium (Ca) did not change, whereas concentrations of immunoreactive insulin (IRI) decreased significantly (P less than 0.01). In response to ISO (0.09 nmol/kg/min) or EGTA (5.6 mumol/kg/min, depressing plasma Ca by 0.27 nmol/l) PTH levels were similarly increased (P less than 0.05) both in the absence and presence of S. On the other hand, S suppressed IRI responses to ISO. During 60-min infusions of EGTA (3.15 mumol/kg/min) plasma Ca fell to significantly lower levels (P less than 0.01) during simultaneous infusions of S than in the absence of exogenous S, while the magnitude of PTH responses was similar. The results do not support a role of somatostatin on basal PTH levels and on PTH responses to beta-adrenergic agonists or hypocalcaemia under conditions, in which S markedly lowers IRI levels and IRI responses to ISO. However, S apparently reduces Ca mobilisation during abrupt hypocalcaemia.
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PMID:Effects of somatostatin on parathyroid hormone levels and on responses of parathyroid hormone to beta-adrenergic agonists and hypocalcaemia. 612 79

The influence of gastrin on intestinal calcium absorption (CaA), serum/plasma insulin, glucagon, parathyroid hormone, calcitonin, glucose, calcium and protein was measured in healthy adult males. Intravenous infusion of pentagastrin (PG. 6 micrograms/kg/h) resulted in a slight decrease of CaA (53.5 +/- (SEM) 5.8% of administered tracer vs. saline control 67.4 +/- 3.4, p less than 0.05). To exclude the influence of hormones like insulin, glucagon and calcitonin stimulated by PG, somatostatin was infused in additional trials. From these experiments and the infusion of synthetic human gastrin-17 (250 ng/kg/h) into 2 subjects, we conclude that acute infusion of gastrin lowers CaA in man.
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PMID:Effects of acutely infused pentagastrin and somatostatin on intestinal calcium absorption in humans. 613 13

Clinical and laboratory data, histologic, electron microscopic and immunocytochemical findings of the tumors of eight patients suffering from Cushing's syndrome and of one patient with hypercalcemia are described. The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Ectopic Cushing's syndrome was caused by pancreatic endocrine tumors, medullary thyroid carcinoma, a bronchial, a gastric and a thymic carcinoid, and a carcinoid of the mediastinum. Hypercalcemia in one patient was related to a pancreatic endocrine tumor. After surgery the clinical symptoms disappeared in two patients, but persisted or relapsed in five patients. ACTH-immunoreactivity could be demonstrated in six of eight tumors; calcitonin-immunoreactivity was found in the tumor of the patient suffering from hypercalcemia. ACTH-immunoreactivity could be localized to secretory granules by immunoelectron microscopy, and the presence of ACTH and beta-LPH in the same tumor cells could be shown in one pancreatic tumor. A combination of production of orthotopic and ectopic hormones was found in one, and secretion of two ectopic hormones was detected in another pancreatic endocrine tumor.
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PMID:Ectopic hormone production by endocrine tumors: localization of hormones at the cellular level by immunocytochemistry. 627 90

An unusual tumor of the cystic duct in a 28-year-old woman is described. The patient presented with a painful distended gallbladder due to a small tumor occluding the cystic duct. Microscopically the tumor cells showed a nesting pattern suggestive of endocrine differentiation, but contained numerous lipid vacuoles and were argentaffin and argyrophil negative. Ultrastructurally, there were relatively few dense granules measuring 135 to 475 nm. Immunoperoxidase staining showed that the tumor cells contained somatostatin but did not contain immunoreactive ACTH, gastrin, calcitonin, glucagon, insulin, parathyroid hormone, or carcinoembryonic antigen. To the authors' knowledge, this is the first reported somatostatinoma occurring in the extrahepatic biliary tract.
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PMID:Somatostatinoma of the cystic duct. 631 50

The effects of salmon calcitonin on the renal concentrating mechanism were investigated in homozygous DI Brattleboro rats. The levels of peptide hormones believed to produce the same physiological responses as antidiuretic hormone on the thick ascending limb (glucagon, parathyroid hormone, and calcitonin) and the cortical collecting ducts (calcitonin) were reduced by acute thyroparathyroidectomy and somatostatin administration. In these hormone-deprived animals, the corticomedullary concentration gradient was almost abolished; the (F/P)osmol at the tip of the juxtamedullary nephrons was 1.19 +/- 0.05. Calcitonin administration restored the gradient [(F/P)osmol = 1.85 +/- 0.14] and simultaneously absolute and fractional water excretion fell significantly despite the concomitant rise in the glomerular filtration rate. It is concluded that 1) in the hormone-deprived animal, calcitonin administration consistently enhances the corticomedullary concentration gradient, and 2) the effects of hormone deprivation and calcitonin administration on the urinary concentrating mechanism are compatible with direct stimulation by calcitonin of electrolyte reabsorption along the thick ascending limb and/or of the water permeability of the cortical collecting ducts.
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PMID:Effects of calcitonin on the renal concentrating mechanism. 662 11

Bombesin, a peptide with widespread biological actions, has been demonstrated in human tissues by immunological methods. To investigate its effect in man, synthetic bombesin was infused at low doses in six male volunteers. Bombesin at 2.4 pmol kg-1 min-1 produced significant rises in plasma insulin, glucagon, pancreatic polypeptide, gastrin, cholecystokinin, motilin, glucose-dependent insulinotropic polypeptide, neurotensin, enteroglucagon, vasoactive intestinal polypeptide, and serum calcium. In contrast, bombesin caused a profound fall in parathyroid hormone levels and reduced plasma glucose concentrations. A late rise in plasma calcitonin was also observed. Bombesin had no significant effect on the pituitary hormones, TSH, GH, PRL, or cortisol. No hormonal changes or alterations in calcium were noted during saline infusions. Bombesin has a marked stimulatory effect on gastrointestinal hormones, which is unique and opposite to the effect of somatostatin, a potent inhibitor of gut hormone release. Bombesin also influences calcium-regulating hormones, either directly or through its action on gut hormones. The bombesin concentrations achieved with the dosages used were low enough to indicate a possible physiological role for the endogenous peptide.
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PMID:Bombesin: action on gut hormones and calcium in man. 706 3

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


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