Disease relevance of SST

• When glucose was infused into dogs with insulin and glucagon levels clamped at basal levels (by means of infusion of somatostatin and replacement of the hormones), RaVLDL increased significantly in the control dogs, but it did not increase further in dogs with sepsis [1].
• In six patients the pain relief was rated "excellent" or "good" and in two patients it was assessed "poor" or "fair". None of the patients demonstrated any evidence of neurologic deficit related to the SST treatment [2].
• Whereas glucose disposal during steady state hyperglycemia was significantly diminished for both PPx and PAT/B in the absence of SST, IIGD was unaltered across all three groups studied [3].
• These results suggest that SST confers better protection against influenza virus infection through augmentation of production of antiviral IgA antibody but not direct action to the virus, and can be used as an adjuvant to nasally inoculated influenza HA vaccine [4].
• Somatostatin (SST) has been shown to induce cholestasis in the dog and in the rat [5].

Psychiatry related information on SST

• To study possible physiologic relationships between somatostatin and the gastric interdigestive contractions (GIC), gastric motor activity, and plasma somatostatin-like immunoreactivity (SLI) concentration were determined simultaneously in four conscious dogs, each of which was studied on two separate occasions [6].
• Decreased somatostatin in the brains of patients with Alzheimer's disease has led to an investigation of the efficacy of neurotransmitter replacement therapy [7].

High impact information on SST

• Somatostatin perfused in canine pancreases at 10 to 20 picograms per milliliter or 10 to 20 percent of the pancreatic vein somatostatin concentration inhibited insulin and glucagon secretion [8].
• The integrity of this separation may determine the sensitivity of islet cells to circulating somatostatin [8].
• Splanchnic somatostatin: a hormonal regulator of nutrient homeostasis [9].
• Somatostatin, a hypothalamic peptide, suppresses hydrochloric acid-stimulated release of secretin, pancreatic flow rate, and bicarbonate and protein secretion in fasted, conscious dogs [10].
• In control dogs glucagon suppression occurred at a glucose level of 150 mg/dl and somatostatin output increased at glucose greater than 250 mg/dl [11].

Chemical compound and disease context of SST

• Glucagon suppression by somatostatin reduces or abolishes hyperglycemia in dogs made insulin-deficient by somatostatin, alloxan, or total pancreatectomy [12].
• After phloridzin pretreatment to eliminate hyperglycemia in the diabetic dogs, insulin and somatostatin suppressed 51 +/- 8 and 31 +/- 10%/h (NS), respectively [13].
• To study the effects of hyperglycemia on the metabolism of alanine and lactate independent of changes in plasma insulin and glucagon, glucose was infused into five 36-h-fasted dogs along with somatostatin and constant replacement amounts of both insulin and glucagon [14].
• Pertussis toxin reversed the ability of somatostatin to inhibit the uptake of [14C]aminopyrine and production of cAMP by parietal cells stimulated with histamine and forskolin but not with dibutyryl cAMP or pentagastrin [15].
• However, after pretreatment of D-cells with pertussis toxin (200 ng/ml), carbachol paradoxically stimulated basal somatostatin release and potentiated the secretagogue action of forskolin [16].

Biological context of SST

• We also examined the effect of low dose morphine on glucose kinetics independent of changes in the endocrine pancreas by the use of somatostatin plus intraportal replacement of basal insulin and glucagon [17].
• Effects of corticotropin-releasing factor on plasma motilin and somatostatin levels and gastrointestinal motility in dogs [18].
• Somatostatin induces ectopic activity fronts of the migrating motor complex via a local intestinal mechanism [19].
• These results indicate that acoustic stress affects gastric and intestinal postprandial motility in dogs, delaying the recovery of the migrating motor complex pattern, inducing a transient slowing of gastric emptying, and enhancing the feeding-induced release of gastrin, pancreatic polypeptide, and somatostatin [20].
• Plasma levels of gastrin, somatostatin, and cholecystokinin immunoreactivity during pregnancy and lactation in dogs [21].

Anatomical context of SST

• It is suggested that the principal mode of action of SST on bile flow is indirect by inhibiting the release of choleretic hormones, whereas SP is suggested to act directly on the hepatocytes [22].
• These results suggest that oral administration of SST shows anti-influenza virus activity in the nasal cavity by activation of T-cell in Peyer's patch lymphocyte and stimulation of production of anti-influenza virus IgA antibody in nasal lymphocyte [23].
• Contribution of the pancreas to circulating somatostatin-like immunoreactivity in the normal dog [24].
• Biosynthesis of somatostatin in canine fundic D cells [25].
• We have measured the contents of somatostatin-like immunoreactivity in the effluent of canine thyroid glands perfused without recirculation with a synthetic buffer medium [26].

Associations of SST with chemical compounds

• The basal serum growth hormone (GH) concentration was markedly elevated (23microg/l) and did not decrease during a glucose tolerance test or after somatostatin administration [27].
• The SST infusion was associated with a pronounced decrease in bile flow and in bile acid secretion and with an increase in bile cholesterol saturation [5].
• Methyl N-[3-[(14 beta-hydroxybufa-4,20,22-trienolid-3 beta-yl)oxy-carbonyl] propanoyl]-L-[3',5'-125I2] diiodotyrosinate ([125I] SST) was used as a radioactive ligand [28].
• After overnight incubation, the antibody-bound and free [125I] SST were separated using polyethylene glycol [28].
• The effect of SST, glucagon, calcitonin and PGE1 on exocrine pancreatic secretion in the unrestrained dog in long-term experiments [29].

Regulatory relationships of SST

• Modulation of motilin-induced somatostatin release in dogs by naloxone [30].
• Somatostatin secretion was inhibited by galanin (p less than 0.001), but not by any of the other investigated peptides [31].
• In an in vitro study, the addition of somatostatin in doses of 0.01 and 0.05 microgram suppressed the renin release in dog renal cortical cell suspension by 74.3% and 53.6%, respectively [32].

Other interactions of SST

• When synthetic somatostatin, a known inhibitor of endogenous motilin release, was infused at a rate that raised the plasma SLI to approximately the levels observed during the contraction period (0.1 microgram/kg per h), the appearance of the subsequent GIC was significantly delayed [6].
• Effect of transforming growth factor alpha and interleukin 8 on somatostatin release from canine fundic D cells [33].
• Intravenous infusions of 50 pmol/kg x h GLP-1 or PYY, which reproduced plasma elevations after intraduodenal fat, inhibited gastric acid secretion by 66 +/- 5% and 51 +/- 6%, respectively (both P < 0.01); coinfusions of GLP-1 and PYY abolished gastric acid secretion (P < 0.001) without influencing plasma gastrin or somatostatin [34].
• Preincubation of cells with somatostatin, N-ethylmaleimide, and (R)-p-cAMPS inhibited galanin- and VIP-induced relaxation [35].

Analytical, diagnostic and therapeutic context of SST

• Because the described neuropathologic changes could also be cancer-related or result from chemotherapy or radiation therapy we suggest that further judicious use of SST is justified in this category of patients, if their pain remains unrelieved despite large doses of opioid analgesics [2].
• Intravenous glucose tolerance tests, with or without a background infusion of somatostatin (SST; 400 ng/kg/min) were performed on all animals preoperatively and postoperatively [36].
• Oral administration of SST (2 g/kg, 18 times) from 7 days before to 13 days after vaccination also significantly augmented serum hemagglutination-inhibiting antibody by nasal inoculation of influenza HA vaccine (5 micrograms/mouse) that was insufficient to induce antiviral antibody [4].
• Secretion at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two- to threefold rise in mean somatostatin release, which persisted throughout the perfusion period [37].
• The somatostatin-like immunoreactivity was studied in dilution experiments and by gel-filtration chromatography, and found to have properties identical to those of synthetic cyclic somatostatin, which was also recovered quantitatively when added to sampling tubes [26].

References