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 recent years a variety of peptide hormones have been isolated from the mammalian hypothalamus and pituitary. Several hypothalamic hormones, including thyroliberin (thyrotropin-releasing factory), luliberin (luteinizing hormone-releasing factor), and somatostatin (somatotropin release-inhibiting factor), have been characterized and synthesized. The subsequent development of radioimmunoassays for these hormones has made possible the study of their physiology. The measurement of prolactin in serum and the release of pituitary hormones after the administration of the hypothalamic hormones has proved to be useful in clinical diagnosis. The use of hypothalamic hormones in treating various clinical disorders and the isolation and characterization of new releasing and inhibiting hormones in the hypothalamus are actively being investigated.
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PMID:Recently discovered hypothalamic-pituitary hormones. 81 15

Specificity of the effect of prostaglandins (PGs) on hormone release by the anterior pituitary gland was studied using cells in primary culture. Growth hormone (GH) release is stimulated by all eight PGs studied, PGE1 and E2 being 1000-fold more potent than the corresponding PGFs. The release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) remains unchanged upon addition of PGEs. While the basal release of thyrotropin (TSH) is only slightly stimulated by concentrations of PGEs above 10(-6)M, an important potentiation of the stimulatory effect of thyrotropin-releasing hormone on TSH release is observed. The release of GH, TSH and LH is stimulated equally well by PGAs and PGBs at concentrations higher than 10(-6)M, 3 X 10(-6)M, and 10(-5)M, respectively. PGFs do not affect the release of any of the measured pituitary hormones at concentrations below 10(-4)M. The stimulation of GH release by PGE2 can be inhibited by the PG antagonist 7-oxa-13-prostynoic acid, a half-maximal inhibition being found at a concentration of 4 X 10(-5)M of the antagonist in the presence of 10(-6)M PGE2. In the presence of somatostatin 10(-8)M, the inhibition of GH release cannot be reversed by PGE2 at concentrations up to 10(-4)M. 8-bromo-cyclic AMP-induced GH release is additive with that produced by PGE2. The present data show that 1) of the five pituitary hormones measured, only GH release is stimulated by prostaglandins at relatively low concentrations, 2) the PGE-induced GH release can be competitively inhibited by 7-oxa-13-prostynoic acid, 3) the inhibition of GH release by somatostatin cannot be reversed by PGE2 and 4) the PGEs increase the responsiveness of the thyrotrophs to TRH.
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PMID:Specificity of the stimulatory effect of prostaglandins on hormone release in rat anterior pituitary cells in culture. 81 70

Passive immunization of rats with an antiserum to synthetic somatostatin caused a 250% elevation of basal serum TSH levels and a nearly 200% increase in TSH-response to TRH. These findings strongly support the concept that pituitary thyrotrophs are regulated by endogenous somatostatin as well as by TRH and thyroid hormones. Serum GH levels in the antiserum-treated rats were considerably higher than those in rats which received normal serum. No clearcut influence on prolactin secretion was observed.
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PMID:Increase in basal and thyrotropin-releasing hormone (TRH)-stimulated secretion of thyrotropin (TSH) by passive immunization with antiserum to somatostatin in rats. 81 48

The prolactin (PRL)-releasing activity of porcine stalk median eminence (pSME) was characterized by an in vivo bioassay and concomitant radioi-munoassay of plasma PRL and thyrotropin (TSH) levels. Methanol extracts of pSME stimulated PRL release in 3-day estrogen-primed rats when administered by the intracarotid route in doses ranging from 0.1 to 2.0 pSME equivalents. Synthetic thyrotropin-releasing hormone (TRH) stimulated the release of PRL and TSH in the dose range of 10 to 300 ng. PRL release was greater in response to a maximally effective dose of pSME than the release elicited by a maximal dose of TRH, and pSME administered together with a greater than mazimally effective dose of TRH caused additional PRL but not TSH secretion. Lysine vasopressin and prostaglandin E1 and E2 stimulated PRL release only at doses several orders of magnitude greater than the dose present in pSME. Somatostatin inhibited the release of TSH but not that of PRL whether the stimulus employed was pSME or TRH. The effective inhibitory dose of somatostatin was also significantly greater than the reported hypothalamic content. When pSME was subjected to incubation with plasma, a treatment reported to inactivate TRH, TSH-releasing activity was destroyed to a greater extent than was PRL-releasing activity. When pSME was adsorbed onto charcoal, the supernatant solution was devoid of TRH, as determined by complete removal of a [3H]TRH marker, yet substantial PRL-releasing activity was retained. TSH-releasing activity eluted from the charcoal with methanol was considerably greater than that expected on the basis of the recovery of [3H]TRH, suggesting the presence in the crude extract of a TSH-release inhibitor or of a TSH-releasing factor other than TRH. Based on the above evidence, we conclude that crude pSME contains PRL-releasing substance(s) distinct from the tripeptide TRH.
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PMID:Dissociation of prolactin-releasing activity from thyrotropin-releasing hormone in porcine stalk median eminence. 81 52

The infusion of linear somatostatin did not block prolactin release induced by either perphenazine, TRH or serotonin. Somatostatin infusion, however, potentiated prolactin release induced by perphenazine and TRH but not that induced by serotonin.
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PMID:The influence of somatostatin on drug-induced prolactin release in the monkey. 82 78

In the present communication, synthetic somatostatin, a hypothalamic factor which has a known inhibitory effect on the release of growth hormone, thyroid-stimulating hormone, prolactin, insulin and glucagon in man and other mammals, was found to have an inhibitory effect on limb and tail regeneration in adult Diemictylus viridescens, when the newts were treated with a daily dose of 3-5 or 15 microgram/animal for a period of 34 days post-amputation. At the higher dose, the animals exhibited total inhibition of appendage regeneration in a few cases and the remainder showed a considerable delay compared to the controls; none of the experimental animals reached the advanced four-digit stage achieved by the controls. Furthermore, the blood glucose and liver glycogen values in the somatostatin-treated animals were significantly lower than the control values. Mechanisms in the storage, mobilization and utilization of glucose (involving hormones) are discussed in relation to appendage regeneration in the newt and possible controls of regeneration at the level of the hypothalamus are suggested.
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PMID:Hormone control in regeneration: effects of somatostatin on appendage regeneration, blood glucose and liver glycogen in Diemictylus viridescens. 91 18

The synthetic linear tetradekapeptide somatostatin (growth-hormone release inhibitory hormone: GHRIH) inhibits the liberation of growth hormone in normal persons in the insulin hypoglycaemia test without influencing the rise of cortisol and prolactin, while the concentrations of LH, FSH and TSH remain unchanged. In patients with florid acromegaly there occurs during administration of GHRIH a marked fall in the raised STH level without influencing the basal level of the other anterior-pituitary hormones. As a further effect there is suppression of the insulin level. The somatostatin at present available has a very short biological half-life and in its present form is, therefore, without therapeutic importance.
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PMID:[The effect of synthetic somatostatin in normal and acromegalic males]. 109 Apr 28

The present concept of growth hormone is not that of an isolated hormone. Growth hormone is closely related to all other parts of system. Chemically, it belongs of to a family of 3 hormones, with prolactin and human placental lactogen. This chemical relationship produces some similar effects. Physiologically, it belongs to a series of hormonal secretions of which the elements are gradually recognized. Above, it is under the control of a releasing factor, still not identified : somatostatin which is an inhibiting factor, tetradecapeptide recently isolated ; below, the majority of the totality of its actions are developped through another hormone, or group of hormones : somatomedine. Present work on this endocrine system suggests new therapeutic prospects.
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PMID:[Current data on growth hormone]. 110 34

Somatostatin, a peptide isolated from ovine hypothalami, prevents growth hormone secretion in vivo and in vitro. Moreover, somatostatin interferes with the secretion of various other hormones: TSH insulin, glucagon, gastrin, VIP and GIP. Under certain conditions a blunting effect on the secretion of prolactin and ACTH can be demonstrated.
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PMID:[Somatostatin -- a review (author's transl)]. 126 5

The acute suppressive effects of L-dopa and somatostatin (growth hormone release inhibiting hormone) on the elevated plasma GH concentrations of seven patients with acromegaly were compared. In addition the effects of the two agents on fasting concentrations of plasma glucose, insulin, glucagon and prolactin were studied. In six of the seven patients hourly samples for GH assay were taken from 08.00 to 20.00 hours on a control day. Synthetic cyclic somatostatin (100 mug) was infused intravenously in an albumin/saline solution over 75 min with a Harvard constant infusion pump. Levodopa 500 mg was given orally. Somatostatin infusion produced a reduction in plasma GH concentrations in six of seven patients (mean reduction 55%). L-Dopa produced a reduction in plasma GH concentrations in the same six patients (mean reduction 52%). The minimum GH concentrations achieved in the two tests were comparable and did not differ significantly from the minimum GH concentrations recorded during the 12 h control study. Mean plasma insulin and glucagon concentrations were also significantly reduced during the somatostatin infusion (P less than 0-025; P less than 0-05 respectively). Plasma glucose concentrations did not change. L-Dopa did not alter mean plasma glucose, insulin or glucagon values. Somatostatin did not alter prolactin values but L-Dopa suppressed basal values to less than 2 ng/ml in five patients. This study shows that the plasma GH change after the administration of L-dopa and somatostatin in acromegaly is comparable and confirms the pancreatic effects of somatostatin.
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PMID:A comparison of the effect of levodopa and somatostatin on the plasma levels of growth hormone, insulin, glucagon and prolactin in acromegaly. 126 63


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