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)

Filtration of basal plasma from normal, alloxan-diabetic, and depancreatized dogs on Bio Gel P-10 yielded four glucagon-immunoreactive fractions. One of them appeared in the true glycagon area with the glucagon-125I (3500 mol vt). Of the other three, one appeared in the void volume (greater than 20000 mol wt), another just before the insulin-125I (congruent to 9000 mol wt), and the last one close to the salt peak (less than 2000 mol wt). The increase of total plasma glucagon immunoreactivity observed in depancreatized and alloxan diabetic dogs was mainly due to an increase in the 3500 and 9000 molecular-weight fractions. Arginine infusion in depancreatized dogs caused an increase in the 3500 molecular-weight fraction. Somatostatin or insulin infusion in depancreatized and alloxan-diabetic dogs resulted in disappearance of the 3500 molecular-weight fraction.
Metabolism 1975 Sep
PMID:Heterogeneity of plasma glucagon immunoreactivity in normal, depancreatized, and alloxan-diabetic dogs. 115 74

Because some baboons repeatedly infused with somatostatin died we reviewed available autopsy material. All six animals chronically treated with somatostatin displayed gross or microscopical pulmonary hemorrhage and increased hemosiderin in lung and liver whereas only one of six untreated animals had a similar abnormality. We therefore examined the hemostatic system in living baboons. Thrombocytopenia (mean platelet count of 84,000 per microliter) was noted in six of seven baboons chronically treated with somatostatin; platelet survival was normal. Clotting factors were unaffected. Fibrinogen concentration and survival were unchanged. The acute effects of intravenous somatostatin (0.8 micrograms per kilogram per minute for two hours) in previously untreated animals transiently decreased platelet count, reduced retention of platelets on glass-bead columns and inhibited aggregation induced by ADP, collagen and epinephrine. Bleeding times were not prolonged. Somatostatin added to platelet-rich plasma in vitro was without effect. These data suggest that prolonged administration of somatostatin should be undertaken with caution.
N Engl J Med 1975 Sep 04
PMID:Effects of somatostatin on hemostasis in baboons. 115 61

Preliminary evidence has suggested that somatostatin might interfere with platelet function in the baboon. Because this agent is currently being administered experimentally to human beings, we studied its effect on coagulation and platelet function in man. In five subjects, a four-hour infusion of somatostatin (500 micrograms per hour) had no definite effect on platelet count, leukocyte count, hematocrit, platelet adhesiveness and aggregation, bleeding time, partial thromboplastin time, prothrombin time, and fibrinogen levels. A similar infusion for 18 hours in three subjects was likewise without effect. These studies indicate that somatostatin does not affect coagulation and platelet function in man and that its prolonged administration lacks ostensible toxicity.
N Engl J Med 1975 Sep 04
PMID:The effect of somatostatin on coagulation and platelet function in man. 115 62

The effect of somatostatin on betazole-stimulated gastric secretion and carbachol-stimulated pancreatic secretion and gall bladder contraction has been studied in seven healthy volunteers. Somatostatin (150 and 250 mug/h) inhibited dose-dependently volume of gastric juice and acid output stimulated by 16 mg betazole. Acid concentration was little affected. 500 mug/h were not more effective than 250 mug/h. Pancreatic secretion stimulated by 250 mug carbachol has been reduced by 80-90% and gall bladder contraction abolished by somatostatin infusion (200 mug/h).
Dtsch Med Wochenschr 1975 Sep 05
PMID:[Effect of somatostatin on betazole-stimulated gastric secretion and carbachol-stimulated pancreatic secretion and gall bladder contraction in man(author's transl)]. 115 80

The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. Concomitantly, there was a marked and prompt reduction of glucagon levels (50%) with a sustained effect. The plasma glucose levels were either unchanged or slightly increased. Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. In all patients, the episodic release of growth hormone seen during the control day was abolished during somatostatin infusion.
J Clin Endocrinol Metab 1975 Sep
PMID:The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus. 115 60

Somatostatin was infused intravenously over two hours to rabbits in a dose of 1.5 mug/kg min with an initial loading dose of 50 mug/kg. This dose inhibited platelet aggregation in response to both ADP and collagen. Lower doses of SRIF had no effect. The addition of SRIF in vitro to either human or rabbit platelet rich plasma also had no effect on collagen or ADP-induced platelet aggregation.
Endocrinology 1975 Sep
PMID:The effect of somatostatin on platelet aggregation. 117 21

The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T 1/2) of 3-4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.
S Afr Med J 1975 Sep 13
PMID:Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease. 117 34

In the present work the effects of the novel neuropeptide Pituitary Adenylate Cyclase Activating Peptide (PACAP) on both AR4-2J cell growth and the modulation of ornithine decarboxylase activity were investigated. Both PACAP38 and the amidated form PACAP27 caused a concentration-dependent stimulation of AR4-2J cell growth; the maximal increase was seen at 1 nmol/L (30% above control, P less than 0.01) with a half-maximal effect at 0.01 nmol/L. Ornithine decarboxylase activity was also increased by PACAP in a dose-dependent manner, reaching half-maximal stimulation at 0.5 nmol/L. The addition of 1 nmol/L of somatostatin analog SMS 201-995 totally suppressed PACAP-stimulated AR4-2J cell growth. Vasoactive intestinal polypeptide (3 mumol/L) and 8-bromo-cyclic adenosine monophosphate (1 mmol/L) had no effect on cell proliferation. Treatment of cells by pertussis toxin (25 ng.mL-1.day-1) suppressed PACAP-stimulated AR4-2J cell growth but enhanced PACAP-induced stimulation of adenylate cyclase activity. It was concluded that PACAP stimulates AR4-2J cell proliferation by a mechanism that seems independent of cyclic adenosine monophosphate production. The mitogenic effect of PACAP depends on a pertussis toxin-sensitive G protein and is associated with an increase of ornithine decarboxylase activity.
Gastroenterology 1992 Sep
PMID:Stimulation of rat pancreatic tumoral AR4-2J cell proliferation by pituitary adenylate cyclase-activating peptide. 132 94

The somatostatin analogue octreotide (SMS 201-995) inhibits secretion and growth of certain tumor cells, and current efforts are directed toward the elucidation of its mode of antiproliferative action. In this study, the effect of octreotide on the growth of ZR-75-1 human breast cancer cells has been characterized in immunodeficient nude mice and in cell culture. These results have been related to the expression of somatostatin receptors in vivo and in vitro. Continuous infusion of 10 micrograms/kg/h of octreotide yielded plasma levels of 5.7 ng/ml and elicited highly significant growth inhibitory effects on solid ZR-75-1 breast tumors in nude mice. After 2 and 4 weeks of treatment, tumor volumes in the octreotide group were 39.1 and 36.7% of those of control animals treated with vehicle, respectively. Autoradiographic studies demonstrated that 8 of 12 ZR-75-1 tumors studied were somatostatin receptor positive. When ZR-75-1 tumor cells were exposed in vitro to nanomolar concentrations of octreotide, a dose-dependent inhibition of cell growth was observed in the presence of 5% fetal calf serum or under serum-free conditions using epidermal growth factor, insulin-like growth factor type I, or insulin as growth stimulus. In parallel receptor-binding experiments, ZR-75-1 cells were shown to express specific high-affinity somatostatin receptors (Kd value = 0.9 nM, Bmax = 6000 sites/cell). From these experiments, we conclude that octreotide is a powerful inhibitor of ZR-75-1 tumor cell growth in nude mice and in culture. This inhibitory action of octreotide and the presence of somatostatin receptors on ZR-75-1 tumor cells in vitro and in vivo suggest a direct, somatostatin receptor-mediated effect of octreotide.
Cancer Res 1992 Sep 15
PMID:Antiproliferative effects of the somatostatin analogue octreotide (SMS 201-995) on ZR-75-1 human breast cancer cells in vivo and in vitro. 132 89

Many cells develop enhanced adenylate cyclase activity after prolonged exposure to drugs that acutely inhibit the enzyme and it has been suggested that this adaptation may be due to an increase in Gs alpha. We have treated wild-type and Gs alpha-deficient cyc- S49 mouse lymphoma cells with a stable analogue (SMS 201-995) of the inhibitory agonist somatostatin. After incubation with SMS for 24 h, the forskolin-stimulated cAMP synthetic rate in intact cyc- cells was increased by 76%, similar to the increase found in the wild-type cells. Forskolin-stimulated adenylate cyclase activity in the presence of Mn2+ was also increased in membranes prepared from SMS-treated cyc- cells; however, guanine nucleotide-mediated inhibition of adenylate cyclase activity was not changed despite a small decrease in inhibitory Gi alpha subunits detected by immunoblotting. Pretreatment of cyc- cells with pertussis toxin prevented SMS from inducing the enhancement of forskolin-stimulated cAMP accumulation in intact cells. After chronic incubation of cyc- cells with SMS, exposure to N-ethylmaleimide, which abolished receptor-mediated inhibition of cAMP accumulation, did not attenuate the enhanced rate of forskolin-stimulated cAMP synthesis compared to N-ethylmaleimide-treated controls. These results with cyc- cells demonstrate that an adaptive increase in adenylate cyclase activity induced by chronic treatment with an inhibitory drug can occur in the absence of expression of Gs alpha.
Cell Signal 1992 Sep
PMID:Prolonged activation of inhibitory somatostatin receptors increases adenylate cyclase activity in wild-type and Gs alpha-deficient (cyc-) S49 mouse lymphoma cells. 132 4


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