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)

Teleost fish osmoregulation is largely the result of integrated transport activities of the gill, gut and renal system. The basic 'epithelial fabric' in each of these tissues is adapted to provide the appropriate transport mechanisms depending upon whether the fish is in fresh water or sea water. Net NaCl transport by the branchial epithelium reverses direction when euryhaline species migrate between the two media, providing a useful focus in experiments designed to elucidate mechanisms of differentiation and integration of transport function. Isolated opercular membranes and skins from certain seawater-adapted species are good models to study branchial salt extrusion mechanisms. These heterogeneous tissues generate short-circuit currents equal to net chloride secretion. The vibrating probe technique has allowed localization of all current and almost all conductance to the apical crypt of chloride cells. Area-specific surface current and conductance of chloride cells are 18 mA cm-2 and 580 mS cm-2 (1.7 omega cm2), ranking them as one of the most actively transporting and conductive cells known. There is no net sodium transport under short-circuit conditions but the chloride secretion process is sodium-dependent and ouabain and 'loop'-diuretic sensitive. Sodium fluxes through chloride cells are large (PNa = 5.2 X 10(-4) cms-1) nd appear passive and rate-limited by a single barrier. A link may exist between the active transport and leak pathways since sodium fluxes always account for 50% of chloride cell conductance. The sodium pathway is probably the chloride cell-accessory cell tight junction, although this is still unresolved. Chloride secretion can be rapidly modulated by several hormones, including catecholamines, somatostatin, glucagon, vasoactive intestinal polypeptide and urotensins I and II. Regulation by these hormones may be by rapid alterations of cellular cAMP levels. Differentiation of chloride cells and chloride secretion may be controlled by cortisol and prolactin. Cortisol stimulates chloride cell proliferation and differentiation and appears to interact with NaCl to initiate salt secretion. Prolactin appears to cause chloride cell dedifferentiation by reducing both the active-transport and leak pathways proportionately.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chloride cells and the hormonal control of teleost fish osmoregulation. 636 Dec 7

Production and release of hormones by the pituitary is known to be under complex hormonal control. Prolactin, for example, is both positively and negatively regulated by steroid and thyroid hormones as well as by peptide hormones. Some hypothalamic releasing factors have been shown to regulate both hormone biosynthesis and hormone release. In the case of growth hormone (GH), glucocorticoids and thyroid hormone stimulate its production, at least in part by stimulating transcription of the GH gene, and somatostatin inhibits and growth hormone-releasing factor (GRF) stimulates its release. So far, however, polypeptide hormone regulation of GH biosynthesis has not been demonstrated. Recently a peptide with GH-releasing activity has been characterized from human pancreatic islet tumours. We report here that pure human pancreatic GRF (hpGRF) stimulates transcription of the GH gene, as well as stimulating GH release.
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PMID:Transcriptional regulation of growth hormone gene expression by growth hormone-releasing factor. 641 87

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

A 20-year-old female presented with thyrotoxicosis associated with amenorrhoea and galactorrhoea after oral contraceptive withdrawal. Serum TSH was persistently elevated (mean: 28 +/- 3.1 microU/ml during 24-h sampling and did not vary significantly after TRH, bromocriptine or somatostatin. Prolactin levels remained constantly at the upper limit of normal (mean: 20.6 +/- 2.1 ng/ml, with a minimal increase after TRH, a slight decrease after somatostatin (54%) and a marked decrease after bromocriptine (88.5%). Surgical exploration revealed an unusually firm tumour adherant to the wall of the sella turcia; electron microscopic study showed that it was composed almost exclusively of thyrotrophs. After a transient period of euthyroidism post-operatively, T3 toxicosis occurred with an increased TSH level (15.5 microU/ml) and a rise in TSH and alpha subunit in response to TRH. An increase in T4 followed while prolactin remained low.
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PMID:Hyperthyroidism due to a pituitary TSH secreting tumour with amenorrhoea-galactorrhoea. 718 98

Female rats were treated in vivo with estrogen for three weeks. The pituitaries were then removed and their responses to somatostatin, dopamine, TRH, hGHRH(1-44)NH2, or their combination were examined in a superfused pituitary cell system. Somatostatin did not decrease basal prolactin secretion in the control cells, but it caused a dose-dependent decrease in prolactin release from the estrogen pretreated cells. Estrogen pretreatment did not alter the sensitivity of pituitary cells to dopamine; dopamine was equally effective in the control and estrogen pretreated pituitaries in decreasing the basal prolactin secretion and TRH induced prolactin release. Prolactin release from the estrogen pretreated cells, stimulated by 25 nM TRH was inhibited by 1 nM somatostatin and nearly totally abolished by 25 nM somatostatin, whereas in the control cells only the higher dose of somatostatin caused some decrease in the prolactin release. Estrogen pretreated cells showed a reduced response to GHRH. Somatostatin did not decrease the basal secretion of GH in either group, but at 1 nM dose it completely abolished the GH release induced by equimolar concentration of GHRH. However, after somatostatin was eliminated from the system, a delayed GH release could be observed that was greater in the control pituitaries than in the estrogen pretreated pituitaries. It is concluded that in vivo treatment with estrogen reduces GH secretion in response to GHRH and increases prolactin secretion after TRH stimulation. After estrogen treatment, the basal and TRH stimulated prolactin release can be effectively reduced by somatostatin. These effects could be observed in vitro using estrogen free tissue culture medium for up to 36 hours after the removal of the pituitaries. The reciprocal changes in GH and prolactin secretion support the concept of the transdifferentiation of GH and prolactin secreting cells.
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PMID:Reciprocal changes in prolactin and growth hormone secretion in vitro after in vivo estrogen treatment. 772 21

The presence of neuropeptide receptors on the plasma membrane is well accepted, as is its internalization and down-regulation. The analysis of the fate of these peptides within their target-cells is difficult. Endogenous peptides or administered native peptides are visualized in these cells using immunocytology after cryoultramicrotomy. Labelled peptides can be injected and their internalization kinetics studied using ultrastructural autoradiography. The pituitary gland is a suitable model for the study of the neuropeptide mechanism, with the lactotroph function being taken as an example in the present case. Prolactin (PRL) release depends on two main neuropeptides: thyrotropin-releasing hormone (TRH) and somatostatin (SS). The TRH immunoreactivity obtained from endogenous as well as injected material was restricted to the plasma membrane, secretory granules, cytoplasmic matrix and nucleus. The internalization kinetics of exogenous native TRH showed an increase of immunoreactive material in all compartments including the nucleus. The endogenous SSs (SS14 and SS28) were detected in the same subcellular lactotroph compartments. Injection of 125I-SS showed a rapid binding of SS at the plasma membrane level before internalization. For 60 min of in vivo uptake, 125I-SS28, the large SS molecule, was detected in the cytoplasm only, while 125I-SS14 was found in the nuclear matrix. In vitro 125I-SS28 was restricted to the nuclear membrane. Under physiological conditions the endogenous neuropeptides were visualized in the nucleus, but after injection of labelled peptides only small molecules were found in the nucleus. The significance of the presence of these neuropeptides is discussed.
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PMID:Internalization and nuclear localization of peptide hormones. 790 23

Availability of recombinant growth hormone (GH) and development of long-acting formulations of this material will undoubtedly lead to widespread use of GH in animal industry and in medicine. GH can act, directly or indirectly, on multiple targets, but its influence on the reproductive system and on the hormonal control of reproduction is poorly understood. Overexpression of GH genes in transgenic animals provides a unique opportunity to study the effects of long-term GH excess. Transgenic mice overexpressing bovine, ovine, or rat GH (hormones with actions closely resembling, if not identical to, those of endogenous [mouse] GH), exhibit enhancement of growth, increased adult body size, and reduced life-span as well as a number of endocrine and reproductive abnormalities. Ectopic overexpression of bovine GH (bGH) driven by metallothionein or phosphoenolpyruvate carboxykinase promoters is associated with altered activity of hypothalamic neurons which produce somatostatin, loss of adenohypophyseal GH releasing hormone (GHRH) receptors, and suppression of endogenous (mouse) GH release. Elevation of plasma levels of GH (primarily bGH) and insulin-like growth factor (IGF-I) in these transgenic mice leads to increases in the number of hepatic GH and prolactin (PRL) receptors, in the serum levels of GH-binding protein (GHBP), in the percent of GHBP complexed with GH, and in the circulating insulin levels. In addition, plasma adrenocorticotropic hormone (ACTH) and corticosterone levels are elevated. Plasma levels of luteinizing hormone (LH), as well as its synthesis and release, are not consistently affected, but follicle-stimulating hormone (FSH) levels are suppressed, apparently due to pre- and post-translational effects. Pituitary lactotrophs exhibit characteristics of chronic enhancement of secretory activity, and plasma PRL levels are elevated. Prolactin responses to mating or to pharmacological blockade of dopamine synthesis are abnormal. Reproductive life span and efficiency are reduced in both sexes, with the severity and frequency of reproductive deficits being related to plasma bGH levels. Most transgenic females expressing high levels of bGH are sterile due to luteal failure. Overexpression of human GH which, in the mouse, interacts with both GH and PRL receptors leads to additional endocrine and reproductive abnormalities including stimulation of LH beta mRNA levels and LH secretion, loss of responsiveness to testosterone feedback, overstimulation of mammary glands, enhanced mammary tumorigenesis, and hypertrophy of accessory reproductive glands in males.
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PMID:Neuroendocrine and reproductive consequences of overexpression of growth hormone in transgenic mice. 807 44

Clinical introduction of octreotide, a long-acting somatostatin analog, has opened a new era in the medical therapy of patients with growth hormone (GH)- and thyroid-stimulating hormone (TSH)-secreting pituitary tumors. Good control of hormonal hypersecretion occurred in most patients, and tumor shrinkage has been observed in more than half of them. Octreotide therapy is of no value in most patients with Prolactin (PRL)- and adrenocorticotrophic (ACTH)-secreting pituitary tumors. However patients with Cushing's syndrome caused by ectopic ACTH secretion from a variety of endocrine tumors benefit from octreotide administration. In patients with visual disturbances related to chiasmal compression by nonfunctioning pituitary tumors, somatostatin analog administration has been reported to result in rapid improvement in visual acuity. This beneficial effect might not be related to a direct action of octreotide, but may reflect an effect on the retina and/or optic nerve. The presence of somatostatin receptors on a wide variety of pituitary tumors as well as on a number of parasellar tumors allows their in vivo visualization with radionucleotide-labelled somatostatin analogs. A positive scan in patients with GH- and TSH-secreting pituitary tumors is predictive of a good suppressive effect of octreotide on hormone release by these tumors. PRL- and ACTH-secreting pituitary adenomas cannot be visualized, but clinically nonfunctioning pituitary adenomas are visualized in 75% of cases with 111In-DTPA-octreotide. At present it is unclear whether this has consequences with regard to the medical treatment of these last group of patients. Somatostatin receptor scintigraphy can be successfully used in the differential diagnosis between pituitary hypersecretion of GH and/or ACTH and the ectopic secretion of growth hormone-releasing hormone (GHRH) and ACTH by peripherally localized endocrine tumors. Again the visualization of such tumors also predicts successful control of hormonal hypersecretion by octreotide.
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PMID:Octreotide and related somatostatin analogs in the diagnosis and treatment of pituitary disease and somatostatin receptor scintigraphy. 809 80

A patient with a macroprolactinoma and extrasellar extension was treated by incomplete transfrontal surgery, external irradiation and additional bromocriptine (Br) treatment. After 4 years, partial bromocriptine resistance developed (a rare occurrence) together with the appearance of intracranial metastases. 123I-Iodobenzamide was helpful in evaluating the dopamine D2 receptor status of the metastatic tumour both in vivo using single-photon emission computed tomography (SPECT) and in vitro. Prolactin release by the cultured metastatic tumour cells was more potently inhibited by CV 205-502 than by bromocriptine. The patient, treated by surgery, irradiation and CV 205-502, developed a ptosis of the left eye and a transient psychiatric delusional state, the latter probably an effect of the dopamine agonist. As the right frontal metastasis was markedly positive on SPECT with 111In-SMS, somatostatin treatment was added to the CV 205-502.
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PMID:Intracranial dissemination of a macroprolactinoma. 810 Nov 48

Pituitary tumours result in hypersecretion of different hormones which can be used in diagnosis. Prolactinomas can be diagnosed by measurement of prolactin serum concentration. Prolactin concentrations of > 150 to 200 micrograms/l are invariably due to macroprolactinoma. Lower levels may indicate microprolactinoma or a peripituitary tumour. Computed tomography scans visualize (micro)prolactinomas of 3 mm. Diagnosis of acromegaly is now based on measurement of serum IGF-I concentration. IGF-I levels correlate with the old test which measured insufficient suppression of GH levels to < 2 micrograms/l in response to oral glucose load. Most endocrine tumours have somatostatin receptors, allowing visualization with radiolabelled somatostatin analogues. 111In-diethylenetriaminopentaacetic acid-octreotide allows normal pituitary and somatostatin positive tumours to be visualized. A positive scan is predictive of good response to octreotide therapy. Cushing's syndrome is diagnosed by ecchymoses, myopathy, hypertension, and by measurement of the overnight 1 mg dexamethasone suppression test, urine cortisol levels and the diurnal cortisol rhythm. Clinically nonfunctioning macroadenomas in post-menopausal women often do not immunostain for gonadotropins. Serum gonadotropin levels are not elevated, although they do release gonadotropins or subunits in vitro. Diagnosis is assisted by TRH administration which increases serum gonadotropins or subunits, especially LH-beta.
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PMID:Current tools in the diagnosis of pituitary tumours. 837 8


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