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)

Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. In pharmacological dosage, gastric acid output, splanchnic blood flow and plasma renin levels, are influenced. A possible therapeutic effect on increased growth hormone secretion, disturbances of carbohydrate metabolism, gastroenteropathies and renal hypertension, is discussed. The clinical application is limited by the short biological half-life of the substance and the unspecific action on several organs.
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PMID:[Somatostatin]. 37 88

This article reviews the current general approach to the biochemical diagnosis and the treatment of pituitary tumors with special reference to medical treatment with dopamine agonists and somatostatin analogs. Dopamine agonists are the treatment of choice in patients with prolactin producing tumors. Octreotide is a major advance in the adjunctive treatment of growth hormone producing tumors. Trans-sphenoidal surgical decompression remains the primary treatment modality in gonadotrofinomas, clinically non-functioning pituitary tumors and thyroid stimulating hormone (TSH) producing tumors. Adrenocorticotrophin (ACTH) producing tumors are treated primarily by selective adenomectomy. The biochemical diagnosis of Cushing's syndrome is complex. Bilateral inferior petrosal sinus sampling for ACTH measurement is highly reliable in the differential diagnosis of ACTH dependent Cushing's syndrome, but needs expertise.
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PMID:Pituitary tumors: diagnosis and treatment. 128 25

Cholinergic mechanisms have been implicated in the regulation of anterior pituitary hormone secretion. The present study was designed to determine the effect of a single injection of an organophosphate acetylcholinesterase inhibitor, diisopropylfluorophosphate (DFP), on anterior pituitary function in male rats. DFP increased serum ACTH (2.7-fold) and corticosterone (9.1-fold), while suppressing TSH, PRL, LH, and GH by up to 95%. The earliest response was at 1 hr, with a duration of at least 18 hr for TSH and LH. Responses were similar in adrenalectomized animals. After DFP, responses to hypothalamic releasing factors were normal for TSH, GH, and ACTH, but significantly blunted for PRL and LH. TSH suppression was partially prevented by combined therapy with a nicotinic (mecamylamine) and a muscarinic (atropine) antagonist. TSH suppression was partially reversed by immunoneutralization with somatostatin antibody, and PRL suppression was completely prevented by a dopamine antagonist (haloperidol). Atropine alone prevented the effects on corticosterone. TSH pituitary content and TSH-beta mRNA were reduced by 37 and 22%, respectively, by DFP. In contrast, PRL mRNA was unchanged but PRL content was increased 3-fold. We conclude that cholinesterase inhibition evokes a multiplicity of effects on anterior pituitary function. There is a hierarchy of responses, with corticosterone being the most and TSH the least sensitive. There is evidence for inhibition at both the hypothalamic and pituitary levels, involving both nicotinic and muscarinic receptors. Although cholinesterase inhibition is the proximate event, other neurotransmitter pathways involved in TSH and PRL suppression are somatostatin and dopamine, respectively.
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PMID:Diisopropylfluorophosphate (DFP) reduces serum prolactin, thyrotropin, luteinizing hormone, and growth hormone and increases adrenocorticotropin and corticosterone in rats: involvement of dopaminergic and somatostatinergic as well as cholinergic pathways. 167 67

Nine patients with psoriasis vulgaris were treated for 12 weeks with somatostatin analog, octreotide acetate (SMS 201-995) 50 or 100 micrograms by subcutaneous injection every 12 hours. The purposes of the study were to determine: (1) levels of insulin, glucose, glucagon, pancreatic polypeptide (PP), and SMS 201-995 after a subcutaneous injection of SMS 201-995 and ingestion of a standardized meal; (2) nocturnal (0200 h) thyroid stimulating hormone (TSH) levels before, during, and after treatment; and (3) the pharmacokinetics of SMS 201-995. Insulin peaks at 30 minutes were blunted from 65.8 +/- 11.0 mu U/mL without treatment to 26.7 +/- 8.6 mu U/mL and 7.7 +/- 2.0 mu U/mL after the 50- and 100-micrograms doses, respectively. Glucagon levels remained constant during the meal and were not affected by the 50-micrograms dose. Mean glucose levels were significantly elevated during insulin suppression. PP was also rapidly suppressed by SMS 201-995 and remained so for 4 hours after the injection. Nocturnal TSH was blunted after 12 weeks of treatment (P less than or equal to .05). T4 and T3 resin uptake showed no depression, and patients remained clinically euthyroid. The plasma peak of SMS 210-995 occurred 30 minutes postinjection and half-life was longer than 2 hours. After chronic administration of SMS 201-995, insulin was suppressed with resultant mild carbohydrate intolerance that persisted throughout the treatment course.
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PMID:Treatment of psoriasis with chronic subcutaneous administration of somatostatin analog 201-995 (sandostatin). II. Effect on pancreatic and thyroid hormone. 240 89

Peptide-hormone- and serotonin-immunoreactive cells of endocrine type are present both in the normal prostatic gland and in the nodules of benign prostatic hyperplasia of man. They are located in the epithelium of the acini and the ducts of all the different parts of the gland, as well as in the urothelium of the prostatic part of the mucosa of the urethra. The endocrine cells are usually argyrophil, sometimes even argentaffin, and immunoreactive with neuron-specific enolase; they can be either of open or of closed type and usually occur widely scattered as single cells. Three kinds of endocrine cells were observed both in the normal gland and in the hyperplastic parenchyma. In the by far most prevalent type serotonin was found to co-exist with a peptide immunohistochemically related to the thyroid stimulating hormone (TSH). In a more rare type serotonin co-existed immunohistochemically with calcitonin. The third kind of endocrine cells was somatostatin-immunoreactive cells; they were also rather rare. The only difference observed between the normal and hyperplastic parenchyma was an increase in the number of all the three kinds of endocrine cells in the hyperplastic nodules. The endocrine cells could easily be visualized by means of silver-staining techniques, even using conventionally formalin-fixed, paraffin-embedded specimens.
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PMID:Peptide-hormone- and serotonin-immunoreactive cells in normal and hyperplastic prostate glands. 243

In order to establish the extent of neuroendocrine differentiation and the occurrence of neurohormonal peptides in the neoplastic cells of prostatic carcinomas, silver-staining and immunocytochemical techniques were used. All gave satisfactory results. The incidence of the neuroendocrine cells seemed to be higher in the fresh "Bouin-fixed" biopsy specimens than in the conventionally "formalin-fixed" specimens from archival paraffin blocks. All carcinomas demonstrated argyrophil cells as an integral element of the tumour. In highly differentiated carcinomas (grade I) these cells were scattered focally, intermingled with non-argyrophil cells in typical adenocarcinomas; their incidence was estimated to be about the same as in benign prostatic hyperplasia. Most of them were immunoreactive with antisera raised against serotonin and/or TSH (thyroid stimulating hormone). In moderately and poorly differentiated (grades II-III) carcinomas, however, the argyrophil cells were more numerous and showed greater variation in growth pattern; only occasionally they displayed a typical carcinoid-like structure. Moderately and poorly differentiated carcinomas also showed a greater variation in the number and kinds of peptide immunoreactivities than the highly differentiated carcinomas. In addition to serotonin- and TSH-immunoreactive cells as the most prevalent type, now also human chorionic gonadotrophin (HCG-alpha), adrenocorticotropic hormone (ACTH), leu-enkephalin, beta-endorphin, somatostatin, glucagon and calcitonin immunoreactive cells could be found within certain tumour areas and often with a distinctly patchy distribution. In two cases, where the tumour cells in the metastases were also investigated, they were found to be both argyrophil and immunoreactive with the same antisera as those of the primary tumour. Our findings emphasise the fact that prostatic carcinomas are more complex and heterogenous than previously thought, exhibiting endocrine differentiation as an integral element of virtually all prostatic adenocarcinomas.
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PMID:Peptide-hormone- and serotonin-immunoreactive tumour cells in carcinoma of the prostate. 244 32

Using sheep thyroid cells in culture, we have studied the effects of thyroid stimulating hormone (TSH), epidermal growth factor (EGF) and the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) on the activity and expression of both thyroglobulin (Tg) and thyroid peroxidase (TPO) and on the ability of cells to trap and organify iodide. Using Western blotting techniques, we found that TSH increased the absolute cellular levels of Tg. The optimum TSH concentration for Tg mRNA production was between 0.1-1.0 mU/ml. Thyroglobulin mRNA levels were stimulated by TSH but detectable levels were also present in cultures grown in its absence containing cortisol, insulin, transferrin, somatostatin and glycyl-lysyl-histidyl acetate. Unlike Tg, TPO protein levels were found to be completely dependent upon TSH. A time course of TSH stimulation of TPO mRNA showed increases after 8 h of TSH stimulation, whereas induction of Tg mRNA by TSH was seen at 24 h. Iodide trapping and organification were also TSH-dependent processes, showing maximum activities at 300-500 muU/ml of TSH. The addition of 10 nM TPA caused a biphasic decrease in radiolabeled pertechnetate uptake, with complete inhibition being seen at 14 h. Inhibition of iodide organification occurred more rapidly. TPA and EGF (1 nM) reduced the amount of newly synthesized Tg in TSH-stimulated cells by 50% but the absolute amount of Tg within the cells was not markedly inhibited at these early times.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of thyroperoxidase, thyroglobulin and iodide levels in sheep thyroid cells by TSH, tumor promoters and epidermal growth factor. 249 23

We have studied the in vitro TSH secretion and the adenylate cyclase (AC) activity of a human pituitary adenoma surgically removed from a hyperthyroid patient showing high serum TSH levels. The tumor appeared almost homogeneously constituted by cells positive for an anti-TSH-beta antiserum and showing the ultrastructural characteristics of the adenomatous thyrotrophs. Adenoma fragments released in vitro a large amount of TSH (148.4 microU/mg prot/30 min), alpha-subunit (35.5 ng/mg prot/30 min) and TSH-beta (10.1 ng/mg prot/30 min). The effects of somatostatin (GHRIH) and dopamine (DA) on the hormone release have been tested in vitro. Both agents markedly inhibited the release of intact TSH and TSH-beta whereas the release of alpha-subunit was less affected. The two agents were effective at concentrations higher than 10(-8)M. The ability of GHRIH and DA in modulating the AC activity was investigated in membrane fraction preparations. GHRIH inhibited AC at concentrations higher than 10(-7)M. The maximal inhibition was 32% at 10(-5)M. Conversely, DA slightly stimulated AC activity. This effects was not mimicked by the dopaminergic ergot CH 29-717, which was completely ineffective on the enzyme. These results suggest that: 1) in this TSH-secreting pituitary adenoma a normal secretory response to the inhibiting agents (GHRIH and DA) is present; 2) different mechanisms of transduction of the GHRIH and DA signals (cAMP dependent and cAMP independent) could be operating in this tumor.
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PMID:In vitro studies on TSH secretion and adenylate cyclase activity in a human TSH-secreting pituitary adenoma. Effects of somatostatin and dopamine. 286 99

Somatostatin has been shown to inhibit the release of various polypeptide hormones including insulin, glucagon, gastrin, thyroid stimulating hormone, and growth hormone. The mechanism by which somatostatin inhibits the release of these various polypeptide hormones has not been fully elucidated. It has been reported that somatostatin increases the level of the second messenger cyclic GMP in rat brain and in the anterior pituitary gland. The present investigation was designed to determine if these responses seen in the anterior pituitary gland and brain were due to activation of guanylate cyclase [GTP-pyrophosphate lyase (cyclizing), E.C.4.6.1.2.], the enzyme that catalyzes the formation of cyclic GMP. Somatostatin at a concentration of 2 pM enhanced guanylate cyclase activity two-fold in rat cerebrum and anterior pituitary gland. This enhancement of guanylate cyclase activity was also seen in rat liver, pancreas, stomach, and small intestine at the same concentration of somatostatin. Increasing the concentration of somatostatin to 20 microM, caused a marked inhibition of guanylate cyclase activity in all these tissues. Dose-reponse curves done on gastric guanylate cyclase activity revealed that over a concentration range of 2 pM to 0.2 microM, somatostatin had a stimulatory effect on guanylate cyclase activity while at concentrations above 10 microM somatostatin was inhibitory to guanylate cyclase activity. The biphasic pattern of enhancement of guanylate cyclase activity at lower concentrations of somatostatin and inhibition at higher concentrations may help to explain some of the discrepancies seen with previous investigations with somatostatin, hormone release, and cyclic nucleotide metabolism.
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PMID:The interrelationship of somatostatin and guanylate cyclase activity. 611 Jan 70

Role of calcium (Ca2+) in the effects of thyroliberin (TRH) and somatostatin (SRIF) on the release of growth hormone (GH), prolactin (PRL) and thyroid stimulating hormone (TSH) from the rat adenohypophyseal cells in primary monolayer cultures has been studied. Decrease of extracellular Ca2+ diminished the stimulatory effects of TRH on TSH and PRL release. Ca2+ is also an important factor in the mechanism of SRIF action. Data obtained in the experiments with high Ca2+ levels in the medium indicate that some antagonistic interrelationship exists between Ca2+ and SRIF. These results suggest that the participation of cAMP alone is not sufficient for stimulus-secretion coupling. Another messenger, namely Ca2+, is necessary for the effects of hypothalamic hormones. On the other hand, the contribution of Ca2+ to the secretory process in mammotrophs, somatotrophs and thyrotrophs is not equal. PRL and TSH secretion is more dependent on the presence of extracellular Ca2+ than the release of GH.
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PMID:Calcium modifies the effects of thyroliberin and somatostatin on hormone release from cell cultures of the rat anterior pituitary. 613 17


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