Immunoreactive Somatostatin Levels Research Articles

Effect of intraventricular injection of neurotensin and other various bioactive peptides on plasma immunoreactive somatostatin levels in rat hypophysial portal blood.

The role of various bioactive peptides in the control of secretion of hypothalamic somatostatin into the hypophysial portal blood was examined in anesthetized rats. Hypophysial portal blood was withdrawn at a rate of 5.0 microliter/min into a chilled tube through a cannula placed over the stump of the pituitary stalk and segmented every 20 min by air bubbles. Immunoreactive somatostatin (IRS) in the plasma was extracted with acetic acid and acetone and quantified by RIA. Basal levels (mean +/- SE) of plasma IRS in the hypophysial portal blood were 646 +/- 36 and 317 +/- 44 pg/ml in urethane- and pentobarbital-anesthetized rats, respectively. Under urethane anesthesia, injection of synthetic neurotensin into the lateral ventricle at various doses in the range of 0.016--2 microgram/rat caused a significant and dose-related increase of plasma IRS levels in the hypophysial portal blood, and this effect of neurotensin was significantly (P less than 0.05) suppressed by pretreatment with diphenhydramine (1 mg/100 g BW, iv), a histamine receptor blocker. Enhancement of IRS release by neurotensin was also observed in pentobarbital-anesthetized rats. Intraventricular injection of substance P (10 microgram/rat), beta-endorphin (1 and 5 microgram/rat), or [Met5]enkephalin had no effect on the level of somatostatin in the hypophysial portal blood of urethane-anesthetized rats. These results suggest a release of hypothalamic somatostatin into the hypophysial portal blood in response to intraventricular administration of neurotensin, probably by a histaminergic mechanism.

Immunoreactive somatostatin in human pancreatic secretion.

Somatostatin in human pancreatic juice collected during endoscopic retrograde cholangiopancreatography following secretin injection was determined by RIA. The mean immunoreactive somatostatin (IRS) levels in the pancreatic juice of 13 non-diabetics was 78 +/- 11 (SE) pg/ml. The IRS levels in 4 non-insulin-dependent diabetics ranged from 843 to 2286 pg/ml with a mean of 1559 +/- 392 (SE) pg/ml. This was significantly greater than non-diabetic values. The IRS in the pancreatic juice was immunologically indistinguishable from somatostatin14 but consisted of 2 major components, one corresponding to somatostatin14 and the other being of a molecular size of approximately 3000 daltons.

Immunoreactive somatostatin distribution and axoplasmic transport in rat peripheral nerve.

The levels of immunoreactive somatostatin (IR-somatostatin) were determined in various parts of the rat spinal cord and peripheral nervous system. The axoplasmic transport rate of IR-somatostatin was determined in the sciatic nerve by the ligation technique. The concentration of the peptide (nanograms per mg protein) was 0.8 ± 0.3 in dorsal root ganglia, 22.1 ± 5.1 in dorsal spinal cord, 5.1 ± 1.2 in ventral spinal cord, and 1.1 ± 0.4 in sciatic nerve. IR-somatostatin was present in a higher concentration in the dorsal root (3.9 ± 1.8 ng/mg protein) than in the ventral root (1.3 ± 0.6 ng/mg protein). Column chromatographic studies showed that most of the IR-somatostatin extracted from dorsal root ganglia and sciatic nerve was identical to the synthetic cyclic somatostatin. In addition, 16% of the total immunoreactivity of the dorsal root ganglia, but not of the peripheral nerve, was of a higher molecular weight form, which probably corresponds to a precursor protein of somatostatin. These observatioons su...

Increased blood somatostatin concentration in streptozotocin diabetic rats

Immunoreactive somatostatin (IRS) was measured and characterized in plasma from the abdominal portel vein (PV) and inferior vena cava (IVC) of normal and streptozotocin diabetic rats. At 1 day following the induction of diabetes, PV and IVC levels of IRS were unchanged, at 2 weeks IVC IRS but not PV IRS was increased, but at 6 months both PV and IVC levels were strikingly elevated. Measurement of the IRS content of the pancreas and gut of the 6 month diabetic group showed a significant increase in the pancreas and stomach but not in the lower gut. Gel filtration of PV plasma from control and chronic diabetic rats revealed 3 immunoreactive forms with apparent m.w. of 12–15 K, 3.6 K and 1.6 K daltons. Immunoreactive somatostatin in the IVC was composed predominantly of the 12–15 K material in normal and diabetic rats. These results suggest that chronic but not acute streptozotocin diabetes leads to increased secretion of IRS from the pancreas and upper gut and to altered peripheral metabolism of IRS. Plasma IRS is heterogeneous, the main component being a high molecular weight form, the concentration of which is markedly increased in chronic insulinopenic diabetes.

The effect of glucose and tolbutamide on immunoreactive somatostatin release from perifused pancreatic islets of normal and streptozotocin diabetic rats.

The patterns of immunoreactive somatostatin (IRS) responses to glucose and tolbutamide were investigated in perifused pancreatic islets of both normal and diabetic rats.The incubation chamber of the perifusion apparatus for the islets was devised with a 2.5 ml disposable syringe. By the method of Lacy, the pancreatic islets were isolated from diabetic rats about 30 days after a single intravenous injection of streptozotocin (STZ, 60 mg/kg body weight) and from normal rats of comparable body weight. The fasting blood glucose was 437±3 mg/100 ml in the diabetic rats and 120±5 mg/100 ml in normal ones. The concentration of IRS in each effluent was measured by the specific double antibody radioimmunoassay for somatostatin.During the initial 20 min incubation period with the medium containing 2.8 mM glucose, the levels of IRS were 11.3±1.0 pg/100 islets/2 min in normal islets and 32.0±3.4 pg/100 islets/2 min in diabetic islets. The latter value was significantly higher than the former (p<0.001). IRS levels gradually rose following 16.7 mM glucose and reached the maximal values with 30.2±5.7 pg/100 islets/2 min at 66 min in normal islets and with 56.8±13.3 pg/100 islets/2 min at 88 min in diabetic islets. The levels of IRS in diabetic islets were significantly higher than those of normal islets (p<0.001) throughout the experimental period. In the case of tolbutamide the IRS levels increased promptly to 51.9±6.6 pg/100 islets/2 min in diabetic islets and to 23.7±4.6 pg/100 islets/2 min in normal islets 2 min after initiation of the infusion. The former value was significantly higher than the latter (p<0.001). The levels of immunoreactive glucagon (IRG) in response to tolbutamide were significantly higher in the diabetic islets than in normal islets (p<0.001). These results indicate that there exists a hypersecrecretion of IRS from STZ-induced diabetic rats during the infusion with glucose and tolbutamide.

Suppression of somatostatin levels in the hepatic portal and systemic plasma of the rat by synthetic human pancreatic polypeptide

Intravenous administration of synthetic human pancreatic polypeptide (hPP) with 36 amino acid residues significantly decreased immunoreactive somatostatin levels in both hepatic portal and systemic plasma in anesthetized rats. The effect of hPP on plasma somatostatin levels is acute. The results suggest that hPP may have a role in controlling somatostatin secretion from the gut and pancreas.

Plasma immunoreactive somatostatin levels in rat hypophysial portal blood: Effect of glucagon administration

Plasma somatostatin levels of the hypophysial portal blood was examined in urethane-anesthetized rats. Portal blood was withdrawn at a rate of 4.7 μl/min via a cannula placed over the stump of the pituitary stalk, collected into the ice-cold tube at 20min intervals before and after the intraventricular injection of test materials. Immunoreactive somatostatin extracted from the plasma with acid acetone was measured by a specific radioimmunoassay. Basal plasma somatostatin concentrations, 778±52pg/ml (means±SE), did not significantly change after the administration of control solution (0.1N acetic acid in physiological saline), while intraventricular injection of glucagon (2, 10 and 50 μg) caused a significant and dose-related increase in plasma somatostatin during the first 20min. These results suggested that somatostatin release from the median eminence into the hypophysial portal vessel was stimulated by glucagon, although the physiologycal significance remains to be clarified.

Immunoreactive somatostatin levels in plasma of normal and alloxan diabetic dogs

Immunoreactive somatostatin levels in plasma of normal and alloxan diabetic dogs

Release of immunoreactive somatostatin from the pancreas in response to glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide.

The effects of glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide upon the release of immunoreactive somatostatin (IRS) from the isolated perfused pancreas were studied. In seven experiments in which glucose was perfused either at a concentration of 100 or 350 mg/dl or at 25 mg/dl, IRS levels were significantly greater at the higher glucose concentrations. In three dose-response experiments in which the perfusing glucose concentration was increased at 30-min intervals from an initial concentration of 25 mg/dl to a final concentration of 300 mg/dl, progressive increases in IRS release were noted at glucose concentrations of 100 mg/dl and above. Perfusion of a 20 mM mixture of 10 amino acids also elicited a prompt and significant biphasic IRS rise in each of six experiments. In five experiments, 20 mM leucine evoked a similar response in mean IRS. Perfusion with 0.075 Ivy U/ml of pancreozymin-cholecystokinin, with or without the presence of a 1 mM 10-amino acid mixture, elicited a prompt rise in IRS with a pattern resembling that of insulin in a total of six experiments. Tolbutamide (0.75 mg/min) also stimulated IRS release in five of six challenges. The IRS responses to nutrients and to pancreozymin and their similarity to the insulin responses raise the possibility that, like insulin, pancreatic somatostatin may have an endocrine role related to nutrient homeostasis.