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)

An invasive TSH-secreting adenoma inducing mild hyperthyroidism was diagnosed in a 16-year-old male. Initial surgical treatment led to a temporary clinical and biological improvement. Recurrence of the thyrotoxicosis was treated with the somatostatin analogue, SMS 201-995 (octreotide) with normalization of the serum thyroid hormone levels with a dose of 200 micrograms per day. With immunoelectron microscopy, the tumour cells appeared poorly granulated with small secretory granules located at the periphery of the cells; only part of those were immunoreactive with an anti-TSH beta monoclonal antibody. No specific TRH binding site was found in a tumour membrane preparation. By quantitative autoradiography, somatostatin specific binding sites were as numerous in the TSH-secreting tumour as in control GH-secreting tumours. Binding kinetics and guanosine triphosphate dependency of the binding were equivalent in the TSH and GH tumours tested. Although all of the tumour cells displayed the same ultrastructural features, some were non-immunoreactive, suggesting that they could secrete an altered form of TSH. The absence of TRH receptors in the tumour cells is in accordance with previous reports on this type of tumour. We confirm the efficiency of octreotide treatment in this case of neoplastic TSH inappropriate secretion. The therapeutic effect of octreotide goes along with the presence of a high density of guanine nucleotide-dependent somatostatin binding sites in the tumour cells.
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PMID:A human TSH-secreting adenoma: endocrine, biochemical and morphological studies. Evidence of somatostatin receptors by using quantitative autoradiography. Clinical and biological improvement by SMS 201-995 treatment. 185 93

Thyrotrophin secreting pituitary adenomas are a rare cause of recurrent thyrotoxicosis. We report on a 47 year old woman with an 8-year history of this condition. In this case the somatostatin analogue, octreotide, normalized thyroid hormone levels. It was associated with marked tumour shrinkage, with striking reduction of the suprasellar extension and improved appearances in the region of the left cavernous sinus shown by high resolution computerized tomography. Following surgery she developed a biochemical relapse which responded to the reinstitution of octreotide. On long term treatment she developed stomach cramps and gallstones. Octreotide was discontinued. We review previous reports of this condition and discuss the role of octreotide in its management.
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PMID:Shrinkage of thyrotrophin secreting pituitary adenoma treated with octreotide. 185 68

Growth hormone (GH) synthesis is known to be impaired by either abnormally high or low levels of thyroid hormone. To determine the effects of these conditions on the central regulation of GH secretion, we have examined their effects on the hypothalamic regulatory peptides GH-releasing hormone (GH-RH) and somatostatin (SRIF). In thyroidectomized rat hypothalamus, a dramatic increase in GH-RH mRNA occurred in parallel with a decrease in peptide content. The significance of this phenomenon is uncertain and might possibly reflect some posttranscriptional derangement of GH-RH synthesis or an increased rate of GH-RH synthesis and release. In the hyperthyroid group, GH-RH showed significant decreases in both peptide and mRNA levels that might possibly reflect a decrease in GH-RH synthesis and secretion. No change was observed in SRIF peptide or mRNA levels in either thyroidectomized or T4-treated animals. As expected, GH mRNA levels in the anterior pituitary were dramatically decreased by thyroidectomy and unaffected by T4 treatment. In addition, in thyroidectomized pituitaries, the mature GH mRNA was observed to alter its structure, increasing in size by approximately 100 nucleotides. This increase in size was found to result from an increase in poly(A) tail length, the significance of which is as yet unclear.
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PMID:The influence of thyroid hormone status on the hypothalamo-hypophyseal growth hormone axis. 196 79

Previous data from our laboratory showed that prolonged exposure of cultural cerebral cortical cells to high potassium concentrations and veratridine resulted in the stimulation of immunoreactive somatostatin (IR-SRIF) synthesis and caused a major increase in its high molecular weight forms. Somatostatin (SRIF) synthesis by cortical and hypothalamic cells was also affected by thyroid hormone (TH). In the present work we have examined to what extent TH might also affect SRIF processing. Cerebral cortical cells maintained as monolayer culture for 7-10 days received triiodothyronine (T3) in concentrations of 10(-11) M and 10(-7) M for 48 h. We found that the total amount of IR-SRIF was increased by high T3 concentrations as reported previously. When the IR-SRIF was characterized by high pressure liquid chromatography (HPLC) or gel filtration, it was evident that thyroid hormone treatment modified the elution profile of IR-SRIF in cells and medium on Bio-Gel P-10 and HPLC, increasing somatostatin 28 (S-28) and decreasing somatostatin 14 (S-14). The results indicate that thyroid hormones affect SRIF processing, leading to a major increase in the synthesis of its high molecular weight forms.
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PMID:Influence of thyroid hormones on somatostatin processing in cultured cerebro-cortical cells. 197 Jan 33

1. Anaesthesia caused marked decreases in the plasma concentrations of triiodothyronine (T3) and thyroxine (T4) and in the body temperature of young fowl. 2. Exogenous T4 or a thyroid hormone secretagogue (somatostatin antiserum), increased endogenous T3 and T4 concentrations and body temperature in conscious birds and prevented the body temperature decline in anaesthetized fowl. 3. These results provide further evidence for a role of T3 and T4 in temperature regulation in birds, particularly during anaesthesia.
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PMID:Thyroid regulation of body temperature in anaesthetized chickens. 197 May 31

In the present study, we investigated whether peptides located within the thyroid gland, but not directly found in nerve fibers associated with blood vessels, might influence thyroid blood flow. Specifically, we evaluated the effects of helodermin, cholecystokinin (CCK), somatostatin (SRIF) and thyrotropin releasing hormone (TRH) given systemically on thyroid blood flow and circulating thyroid hormone levels. Blood flows in the thyroid and six other organs were measured in male rats using 141Ce-labeled microspheres. Circulating thyrotropin (TSH) and thyroid hormone levels were monitored by RIA. Helodermin (10(-10) mol/100 g BW, i.v. over 4 min) markedly elevated thyroid blood flow (52 +/- 6 vs. 10 +/- 2 ml/min.g in vehicle-infused rats; n = 5). Blood flows to the salivary gland, pancreas, lacrimal gland and stomach (but not adrenal and kidney) were also increased during helodermin infusions. CCK, SRIF, and TRH were without effect on blood flows to the thyroid and other organs even though these peptides were tested at higher molar doses than helodermin. Helodermin, CCK, or SRIF did not affect thyroid hormone or plasma calcium levels. As expected however, plasma TSH and T3 levels were increased at 20 min and 2 h, respectively, following TRH infusions. Since helodermin shares sequence homology with VIP, we next compared the relative effects of these two peptides on thyroid and other organ blood flows. VIP (10(-11) mol/100 g BW, i.v.) was more potent in increasing blood flows to the thyroid, salivary gland, and pancreas than an equimolar dose of helodermin. This study shows that while helodermin, like VIP, has the ability to increase thyroid and other organ blood flows, it appears to be a less potent vasodilator.
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PMID:Helodermin, but not cholecystokinin, somatostatin, or thyrotropin releasing hormone, acutely increases thyroid blood flow in the rat. 198 23

Whenever abnormal hormone values are found in a patient, it is necessary to inquire whether medicaments may be implicated. Some of the mechanisms of drug induced hormonal alterations are presented, and drugs which affect and alter prolactin, TSH, thyroid hormones and (in brief) GH and ACTH are summarized and discussed for the non-specialist. Hyperprolactinemia is caused by estrogens, neuroleptics and other dopaminantagonists, antidepressants, opioids, reserpine, a-methyl-dopa, H2-receptor blockers, etc. Serum TSH is decreased by glucocorticoids, somatostatin, dopaminergic agents, a-adrenergic blockers, etc., and increased by neuroleptics and other dopamin antagonists, cimetidine, clomiphene, spironolactone, etc. Thyroid hormones are altered by agents which inhibit thyroid hormone synthesis or secretion (thionamides, some sulfonamides; lithium), which increase (estrogens, methadon) or decrease (androgens, glucocorticoids) the concentration of TBG (thyroxine binding globulin), which competitively inhibit thyroid hormone binding to TBG (salicylates, phenytoin, etc.), and which inhibit the conversion of T4 to T3 (beta-adrenergic blockers, amiodarone, glucocorticoids) or stimulate degradation or fecal excretion of thyroid hormones (rifampicin, phenytoin, carbamazepine). For some drugs, in particular those with multiple effects on one or several endocrine systems, the only safe test which definitely allows drug-induced hormonal disturbances to be confirmed or ruled out is withdrawal of the drug and repetition of the hormone measurement.
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PMID:[Abnormal hormone values: do drugs play a role? Abnormal prolactin, TSH and thyroid hormone values]. 216 99

We report a case of hyperthyroidism due to inappropriate thyrotrophin (TSH) secretion in a patient with selective pituitary resistance to thyroid hormone action. Symptoms of hyperthyroidism in patients with this disorder are usually mild, implying some peripheral tissue resistance to the metabolic effects of thyroid hormone. Our patient had unusually severe symptoms, including marked weight loss and cardiac arrythmias which required carbimazole and beta-blocker therapy for control. Somatostatin was ineffective in suppressing TSH secretion. The introduction of sensitive thyrotrophin assays should facilitate the accurate diagnosis of TSH-induced hyperthyroidism and avoid inappropriate treatment.
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PMID:Clinical hyperthyroidism due to non-neoplastic inappropriate thyrotrophin secretion. 223 9

The management of hyperthyroidism due to inappropriate secretion of TSH (IST) includes agents that selectively suppress TSH hypersecretion both in patients with TSH-secreting tumor [neoplastic IST (nIST)] in whom pituitary surgery was unsuccessful and in those with selective pituitary resistance to thyroid hormone action [nonneoplastic IST (nnIST)]. Among such agents, somatostatin administration has proven to be effective in blocking TSH hypersecretion, but its short plasma half-life prevented its use in long term therapeutic trials. The recent availability of a potent and long-acting analog of somatostatin (SMS 201-995, Sandostatin) prompted us to study its effects on serum TSH, alpha-subunit, and free thyroid hormone (FT4 and FT3) concentrations in five patients with nIST and three patients with nnIST. During short term SMS 201-995 administration (100 micrograms, sc, three times daily for 5 days) both serum TSH and alpha-subunit levels decreased in all patients with nIST (mean decrements, -86% and -85%, respectively), with concomitant normalization of serum FT4 and FT3 concentrations. In the three patients with nnIST, this treatment lowered serum TSH levels less well (mean decrement, -47%), although serum FT4 and FT3 levels normalized in one patient. Chronic SMS 201-995 (100 micrograms, sc, every 12 h for 1-7 months) treatment in four hyperthyroid patients (two with nIST and two with nnIST) resulted in a steady euthyroid state in both patients with nIST, with restoration of normal visual fields in one patient. In contrast, in both patients with nnIST, escape occurred after 2 weeks of therapy. We conclude that SMS 201-995 administration is effective treatment for patients with nIST, able to suppress TSH hypersecretion from the adenomatous thyrotrophs and, consequently, to restore clinical and biochemical euthyroidism in such patients. On the contrary, the inhibitory effects of SMS 201-995 on TSH secretion in patients with nnIST are weaker and transient.
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PMID:Treatment of hyperthyroidism due to inappropriate secretion of thyrotropin with the somatostatin analog SMS 201-995. 249 62

It seems clear from the studies reviewed here that there is adequate evidence to support the concept of a biphasic response of the thyroid gland to cold as first postulated by Moll et al. (1972). The initial response to acute exposure to cold begins at the level of the hypothalamus as a result of either neural stimuli from skin and other areas and/or blood of somewhat lower than normal temperature reaching the hypothalamus (Andersson et al., 1963). As a result, the secretion of norepinephrine and/or dopamine may increase, and serotonin and/or somatostatin may decrease. The net result of these is an increase in the release of TRH from the hypothalamus. This, in turn, stimulates the cascade for the release of TSH from the anterior pituitary gland and thyroid hormone from the thyroid gland. Moll et al. (1972) postulated the lack of a feedback limb in this acute phase, and, indeed, this may be the case. It is possible, however, that certain hormones, such as somatostatin, norepinephrine, T3, and T4 could act in the capacity of feedback inhibitors. Additional experiments will be required to assess this possibility. The transitional link between the acute (less than 1 day) and chronic (greater than 1 day) phases of the response of the thyroid gland to cold could be T4 itself. An increase in the concentration of T4 in plasma has been reported to increase peripheral deiodination of T4 to T3 by kidneys and liver of rats. There are no studies at present to indicate that hepatic conjugation can be increased by elevation of plasma levels of T4 and T3. If it can, these responses would provide adequate reasons as to why peripheral metabolism of thyroid hormones increases during chronic exposure to cold. The time-course for these changes to occur needs to be studied in greater detail to establish the sequence of events following acute exposure to cold. The latter may also increase urinary excretion of T4 and T3 in man, but not the rat. This suggests that another aspect of exposure to cold needing additional study is measurement of the binding affinities of T4 and T3 for their transport proteins during exposure to cold as compared to affinities prior to exposure to cold. If binding affinities are reduced, the amount of free hormones would increase and, consequently the likelihood of being excreted into urine and conjugated by the liver would also increase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Activity of the hypothalamic-pituitary-thyroid axis during exposure to cold. 265 59


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