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)

In order to investigate whether somatostatin plays a role in the regulation of thyroid hormone secretion we have compared the effects of a prolonged somatostatin infusion on insulin and glucagon levels, on the one hand, with its effect on T4, T3, rT3 and TSH, on the other. Furthermore, the serum levels of somatomedin A were determined. Saline was infused in control experiments. Cyclic somatostatin was given as an i.v. bolus of 200 micrograms followed by a constant rate infusion of 50 micrograms/h during 24 hours. Somatostatin suppressed basal insulin and glucagon levels as well as insulin responses to meals but did not influence somatomedin A levels. T4 and T3 decreased during the first hour, whether somatostatin was given or not. Thereafter, T4 and T3 remained stable in the control experiments, while they continued to decrease slowly when somatostatin was added. The suppressive effect of somatostatin was significant 11 hours (p less than 0.05) and 24 hours (p less than 0.005) after the onset of the infusion. In contrast, rT3 and TSH were not suppressed by somatostatin. The fact that basal TSH did not decrease, favors the idea that the suppression of T4 and T3 was mainly due to a direct inhibitory effect of somatostatin on the thyroid gland. Our observation that a low dose of somatostatin decreases peripheral T4 and T3 levels supports the idea that somatostatin plays a role in the regulation of thyroid hormone secretion.
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PMID:Effect of 24-hour somatostatin infusion on glucose homeostasis and on the levels of somatomedin A and pancreatic and thyroid hormones in man. 39 78

Somatostatin was infused in various doses into normal subjects and juvenile diabetics for a 24-hour period preceded by a 24-hour control period and followed by another three-hour control period. Saline was infused during the first control period. Meals were served during the two 24-hour periods. Blood samples were taken hourly. Five normal males received a total dose of 4 mg. somatostatin. Four male diabetics received 2 mg., four received 4 mg., and four 6 mg. In the diabetics, somatostatin suppressed plasma growth hormone, glucagon, and glucose throughout the infusion. All parameters rebounded at cessation of infusion. In the normals, somatostatin suppressed plasma growth hormone, glucagon, and insulin but increased plasma glucose. It is concluded that the plasma glucose suppression in the diabetics is mainly due to the suppression of the diabetogenic hormones growth hormone and glucagon. A minor effect of decreased and/or delayed absorption of carbohydrates cannot be excluded in these experiments. The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion.
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PMID:24-hour studies of the effects of somatostatin on the levels of plasma growth hormone, glucagon, and glucose in normal subjects and juvenile diabetics. 64 Feb 35

In order to assess the ability of nicotinic acid to decrease plasma glucose concentration, normal individuals were given continuous four hour infusions of either nicotinic acid (NA), somatostatin (SRIF), NA + SRIF, or 0.9% NaCl (Saline). Plasma non-esterified fatty acid (NEFA) concentration decreased to about one-fourth of the basal value in response to either NA or NA + SRIF, associated with statistically significant decreases in plasma glucose concentration. The ability of NA and NA + SRIF to decrease plasma glucose concentration was seen despite the fact that plasma insulin concentrations also fell significantly during both infusions. Although plasma glucose concentration fell significantly in response to both NA and NA + SRIF, the effect of NA + SRIF was approximately twice as great as that seen with NA alone. The augmented hypoglycaemic effect of NA + SRIF as compared to NA alone was associated with a concomitant fall in plasma glucagon concentration. In contrast, plasma glucose concentration did not change following Saline, and was actually higher than baseline after the infusion of SRIF alone. These results provide evidence that NA can lower plasma glucose concentration in normal volunteers, and suggests that this is mediated by the NA-associated decrease in plasma NEFA concentration.
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PMID:Effect of nicotinic acid on plasma glucose concentration in normal individuals. 135 76

The purpose of this study was to determine the heart rate and arterial blood pressure changes to isometric skeletal muscle contraction and muscle stretch before and after microinjecting an antagonist to substance P (SP) or somatostatin (SOM) into the L-7 dorsal horn region of the spinal cord of anesthetized cats. Anesthesia was induced by administering an anesthetic gas mixture and was subsequently maintained with alpha-chloralose. Triceps surae contraction was induced by electrically stimulating the L-7 ventral root. Three muscle manipulations (all 1 minute in duration) were performed: 1) continuous tetanic contraction, 2) intermittent tetanic contractions (1 second of contraction, 1 second of relaxation), and 3) passive muscle stretch. Saline microinjections had no effect on the cardiovascular responses to these muscle manipulations. However, both peptide antagonists blunted the pressor response to a continuous tetanic contraction as mean arterial pressure increased 47 +/- 4 and 44 +/- 4 mm Hg before and 28 +/- 3 and 28 +/- 4 mm Hg after microinjecting the SP or SOM antagonist, respectively. In contrast, neither antagonist influenced the increase in mean arterial pressure produced by passive stretch; values were 43 +/- 6 versus 41 +/- 6 mm Hg (SP antagonist) and 39 +/- 7 versus 42 +/- 7 mm Hg (SOM antagonist) before and after injections, respectively. Microinjecting the SOM antagonist attenuated the pressor response to intermittent tetanic contractions (44 +/- 4 mm Hg before SOM antagonist versus 26 +/- 4 mm Hg after SOM antagonist), whereas the SP antagonist had no effect (35 +/- 3 mm Hg before SP antagonist versus 32 +/- 4 mm Hg after SP antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex. 137 Sep 23

The effects of i.v. administration of thyrotrophin-releasing hormone (TRH) and of somatostatin on circulating plasma levels of porcine GH in the chronically catheterized pig fetus have been examined. Growth hormone levels increased markedly (P less than 0.01) following TRH administration, but there was no change in thyroxine levels by 1 h after treatment. Administration of somatostatin caused a significant (P less than 0.05) decrease in mean GH levels, but the response was variable between pigs. Saline administration had no significant effect on GH levels. These results suggest that the mechanisms regulating postnatal GH release are present in the fetal pig, but may not be fully developed 8-12 days before delivery.
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PMID:Effect of somatostatin and thyrotrophin-releasing hormone on the levels of growth hormone in the circulation of the chronically catheterized pig fetus in utero. 286 13

To study the effect of insulin on leucine kinetics, three groups of conscious dogs were studied after an overnight fast (16-18 h). One, saline-infused group (n = 5), served as control. The other two groups were infused with somatostatin and constant replacement amount of glucagon; one group (n = 6) received no insulin replacement, to produce acute insulin deficiency, and the other (n = 6) was constantly replaced with 600 muU/kg per min insulin, to produce twice basal hyperinsulinemia. Hepatic and extrahepatic splanchnic (gut) balance of leucine and alpha-ketoisocaproate (KIC) were calculated using the arteriovenous difference technique. l,4,5,[(3)H]Leucine was used to measure the rates (micromoles per kilogram per minute) of appearance (Ra) and disappearance (Rd), and clearance (Cl) of plasma leucine (milliliters per kilogram per minute). Saline infusion for 7 h resulted in isotopic steady state, where Ra and Rd were equal (3.2+/-0.2 mumol/kg per min). Acute insulin withdrawal of 4-h duration caused the plasma leucine to increase by 40% (P < 0.005). This change was caused by a decrease in the outflow of leucine (Cl) from the plasma, since Ra did not change. The net hepatic release of the amino acid (0.24+/-0.03 mumol/kg per min) did not change significantly; the arterio-deep femoral venous differences of leucine (-10+/-1 mumol/liter) and KIC (-12+/-2 mumol/liter) did not change significantly indicating net release of the amino and ketoacids across the hindlimb. Selective twice basal hyperinsulinemia resulted in a 36% drop in plasma leucine (from control levels of 128+/-8 to 82+/-7 mumol/liter, P < 0.005) within 4 h. This was accompanied by a 15% reduction in Ra and a 56% rise in clearance (P < 0.001, both). Net hepatic leucine production and net release of leucine and KIC across the hindlimb fell markedly. These studies indicate that physiologic changes in circulating insulin levels result in a differential dose-dependent effect on total body leucine metabolism in the intact animal. Acute insulin withdrawal exerts no effect on leucine rate of appearance, while at twice basal levels, insulin inhibited leucine rate of appearance and stimulated its rate of disappearance.
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PMID:Role of insulin in the regulation of leucine kinetics in the conscious dog. 612 47

Five female acromegalic patients who had undergone surgical adenomectomy, but still had elevated hGH serum levels, were treated with bromocriptine, 5-15 mg daily, for at least 4 months without a satisfactory response. In an attempt to lower serum hGH levels, p-NH2-Phe4-D-Trp8-somatostatin was administered, 100 micrograms as an i.v. bolus, followed by infusion of 250 micrograms over a 4 hour period. The analogue decreased hGH levels by about 50% in 3 out of 5 patients, both during bromocriptine treatment and also in its absence. Of the remaining two patients, one showed a decrease in hGH levels in response to the analogue only during bromocriptine treatment and the other only without it. Saline infusion after bromocriptine administration did not induce a decrease in hGH levels in three of these patients. Somatostatin analogue caused a fall in serum insulin levels in all but one patient, who had diabetes mellitus and in whom serum insulin was undetectable. Both hGH and insulin levels showed a significant rebound after infusion of the analogue, but returned to basal levels within 24 hours. Prolactin did not change during the analogue infusion in 4 patients with normal PRL levels. However, in one patient in whom prolactin and hGH levels were elevated during bromocriptine treatment, the infusion of somatostatin analogue decreased both hormones. The analogue induced no changes in serum TSH, FSH and LH levels of any of the patients.
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PMID:Effect of a somatostatin analogue on trophic hormone levels in acromegalic patients with elevated hGH after adenomectomy and treatment with bromocriptine. 654 82

Interruption of a chronic GABA infusion into the rat somatosensory cortex induces the appearance of focal epileptic manifestations, known as the 'GABA withdrawal syndrome' (GWS). The aim of the present study was to determine, by immunocytochemistry, if neurotransmitters other than GABA are involved in GWS, namely: noradrenaline (NA), serotonin, choline acetyltransferase (CAT), cholecystokinin, neuropeptide Y, somatostatin and glial fibrillary acid protein (GFAP). Immunocytochemical data were compared in three animal groups: GABA-, saline- and L-aspartate (L-Asp)-infused rats. Only GABA-infused rats presented epileptic manifestations after interruption of the infusion. Saline- and L-Asp-infused rats served as controls. Observations were limited to the region surrounding the cortical infusion site. GABA-infused rats showed in the zone of the epileptic focus a number of cell bodies strongly immunoreactive to NA antibodies much larger than control rats. In addition, NA-immunoreactive fibers formed a dense plexus and some of them were observed around perikarya. In saline- and L-Asp-infused rats, the NA-immunolabelled fibers were sparse and NA immunolabelling was rarely observed in cell bodies. These results contrast to those obtained for the serotonergic system, where no significant difference was observed among the three groups of rats. CAT immunolabelling was observed in cell bodies, but not in nerve terminals in rats of the three groups. The number of CAT-immunoreactive cell bodies was much greater in GABA-infused rats than in the control animals. GFAP immunolabelling showed an important number of astrocytes throughout the cortex of the GABA-infused hemisphere, whereas, astrocytic reaction was limited to the infusion site in controls. Immunocytochemical data concerning peptides revealed cortical neuronal elements labelled similarly in the three groups of rats. Noradrenergic, cholinergic and glial modifications observed mainly in GABA-infused rats can result from lesion and from a specific action of GABA in chronic infusion. These modifications may contribute to the epileptogenesis of GWS, as recently demonstrated by electrophysiological recordings that show a modulating action of NA on firing activity of neurons involved in the epileptic focus.
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PMID:High expression of noradrenaline, choline acetyltransferase and glial fibrillary acidic protein in the epileptic focus consecutive to GABA withdrawal. An immunocytochemical study. 781 66

The effect of lactate per se on alanine and glucose metabolism was studied in five overnight-fasted conscious dogs. Somatostatin was infused to inhibit endogenous pancreatic insulin and glucagon release and the hormones were replaced intraportally at basal rates. Saline (n = 5) or lactate (at 25 and 50 mumol.kg-1.min-1 for 90 minutes each) was infused, and blood samples were taken during the last 30 minutes of each 90-minute period. Insulin, epinephrine, norepinephrine, and cortisol levels remained unchanged during saline or lactate infusion. Glucagon level decreased slightly during lactate (94 +/- 7 to 74 +/- 9 and 79 +/- 8 pg/mL) and saline (91 +/- 8 to 90 +/- 4 and 81 +/- 11 pg/mL) infusions. There were no significant changes in lactate or alanine levels or net hepatic balances with saline infusion. Blood lactate level increased from 657 +/- 74 to 1,718 +/- 126 and 3,300 +/- 321 mumol/L (both P < .05) during the low- and high-lactate infusion periods, respectively. The liver produced lactate during the control (5.57 +/- 2.92 mumol.kg-1 x min-1) and low-lactate infusion (1.75 +/- 2.58 mumol.kg-1 x min-1) periods, but consumed lactate (3.89 +/- 3.31 mumol.kg-1 x min -1; P < .05) during the high-lactate infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of lactate loading on alanine and glucose metabolism in the conscious dog. 847 11

Octreotide inhibits the secretion of several hormones and exerts vasopressor effects. To clarify the mechanism of atrial natriuretic factor (ANF) secretion and to assess the cardiovascular effects of octreotide in relation to changes in vasoactive peptide secretion, four groups of conscious dogs were studied: group I (n = 11) received saline infusion after placebo, group II (n = 10), the same infusion after octreotide, group III (n = 10), placebo only and group IV (n = 10) octreotide injection only. Saline (10% body wt) was infused over 40 min after subcutaneous injection of placebo or octreotide (1 microgram/kg). Saline produced a rise (p < 0.001) of plasma ANF from 32.4 +/- 4.1 to 59.0 +/- 8.5 pM after placebo and from 35.6 +/- 5.5 to 77.0 +/- 12.6 pM after octreotide. This rise, not significantly different between groups I and II paralleled a 4-5-fold increase (p < 0.005) of right and left atrial pressures. With a higher dose of octreotide (4 micrograms/kg) injected in 4 dogs, plasma ANF increased by 27.5 +/- 5 pM. During hypervolemia, plasma endothelin-1 remained unchanged but plasma angiotensin II and epinephrine decreased (p < 0.05) approximately by 80% without being affected by octreotide. Octreotide did not influence the basal secretion of ANF, endothelin-1, angiotensin II and catecholamines. However, in basal conditions, octreotide injection resulted in a 9% increase (p < 0.005) of left ventricular systolic pressure, unobserved after placebo. Plasma glucose decreased (p < 0.005) in groups receiving octreotide. Thus, octreotide does not impair the stretch-mediated release of ANF which implies a release mechanism independent from somatostatin receptors and consequent changes in intracellular c-AMP. Octreotide has also a pressor effect, unrelated to changes in vasoactive peptide production.
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PMID:Effects of octreotide on cardiovascular hormones and haemodynamics in conscious dogs. 877 62


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