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)

The effect of somatostatin on thyroid hormone secretion stimulated by TSH in man was studied. The injection of TSH into a thyroid artery during surgery was followed by an increase in the serum concentration of iodothyronines in the corresponding thyroid vein. This increase was significantly lower (p less than 0.02) when somatostatin was given as a bolus injection into a peripheral vein 5 min prior to the administration of TSH, and followed by a continuous infusion for 60 min. Since somatostatin-like immunoreactivity has been localized to some cells of the thyroid gland being in a parafollicular location, it is suggested that somatostatin may be an intrathyroidal regulator of thyroid activity in man.
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PMID:Somatostatin inhibits thyroid hormone secretion induced by exogenous TSH in man. 4 73

The recent discovery of somatostatin-containing cells within the thyroid gland infers that somatostatin may influence thyroid activity. This possibility was investigated by measurements of radio-iodine release in mice pre-treated with 125I and T4. The animals were treated with TSH, isoprenaline or dibutyryl-cyclic AMP with and without concomitant injection of somatostatin. It was found that somatostatin reduced the blood 125I increase in response to each of the three thyroid-stimulating agents. The elimination rates of 125I-labelled T4 and T3 were unaffected by somatostatin. The observations suggests that somatostatin may participate in the regulation of thyroid hormone secretion, by an inhibitory effect exerted within the thyroid gland.
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PMID:Inhibition by somatostatin of mouse thyroid activity following stimulation by thyrotrophin, isoprenaline and dibutyryl cyclic-AMP. 19 13

In order to investigate whether somatostatin plays a role in the regulation of thyroid hormone secretion we have compared the effects of a prolonged somatostatin infusion on insulin and glucagon levels, on the one hand, with its effect on T4, T3, rT3 and TSH, on the other. Furthermore, the serum levels of somatomedin A were determined. Saline was infused in control experiments. Cyclic somatostatin was given as an i.v. bolus of 200 micrograms followed by a constant rate infusion of 50 micrograms/h during 24 hours. Somatostatin suppressed basal insulin and glucagon levels as well as insulin responses to meals but did not influence somatomedin A levels. T4 and T3 decreased during the first hour, whether somatostatin was given or not. Thereafter, T4 and T3 remained stable in the control experiments, while they continued to decrease slowly when somatostatin was added. The suppressive effect of somatostatin was significant 11 hours (p less than 0.05) and 24 hours (p less than 0.005) after the onset of the infusion. In contrast, rT3 and TSH were not suppressed by somatostatin. The fact that basal TSH did not decrease, favors the idea that the suppression of T4 and T3 was mainly due to a direct inhibitory effect of somatostatin on the thyroid gland. Our observation that a low dose of somatostatin decreases peripheral T4 and T3 levels supports the idea that somatostatin plays a role in the regulation of thyroid hormone secretion.
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PMID:Effect of 24-hour somatostatin infusion on glucose homeostasis and on the levels of somatomedin A and pancreatic and thyroid hormones in man. 39 78

The hypothalamic factors dopamine (DA) and somatostatin (SRIH) inhibit pituitary glycoprotein secretion, but little is known regarding the effects of these factors on glycoprotein pulses. To address this question, 12 healthy volunteers underwent frequent blood sampling over 12 h at baseline and during 12-h infusions of DA and/or SRIH. TSH, LH, FSH, and alpha-subunit (alpha) levels were measured in all samples, and hormone pulses were located by Cluster analysis. Both DA and SRIH suppressed TSH pulse amplitude by 70%, while SRIH decreased TSH pulse frequency as well. Both infusions decreased LH pulse amplitude by 30-35%, but had no effect on pulse frequency. In contrast, neither infusion significantly altered FSH pulse parameters, although mean FSH levels declined 15%. DA had no effect on pulsatile alpha secretion, while SRIH decreased alpha pulse frequency. Serum thyroid hormone levels declined during both infusions, but there were no major changes in serum sex steroid levels. Thus, the hypothalamic inhibitory factors DA and SRIH had divergent effects on glycoprotein hormone pulses. The major effects on pulse amplitude, rather than frequency, imply that these factors do not play major roles in the generation of glycoprotein pulses, although SRIH may directly affect the TSH and alpha pulse generators.
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PMID:Effects of dopamine and somatostatin on pulsatile pituitary glycoprotein secretion. 134 83

The effect of thyroid hormone deficiency and growth hormone (GH) treatment on hypothalamic GH-releasing hormone (GHRH)/somatostatin (SS) concentrations, GHRH/SS mRNA levels, and plasma GH and somatomedin-C (IGF-I) concentrations were studied in 28- and 35-day-old rats made hypothyroid by giving dams propylthiouracil in the drinking water since the day of parturition. Hypothyroid rats, at both 28 and 35 days of life, had decreased hypothalamic GHRH content and increased GHRH mRNA levels, unaltered SS content and SS mRNA levels, and reduced plasma GH and IGF-I concentrations. Treatment of hypothyroid rats with GH for 14 days completely restored hypothalamic GHRH content and reversed the increase in GHRH mRNA, but did not alter plasma IGF-I concentrations. These data indicate that, in hypothyroid rats, the changes in hypothalamic GHRH content and gene expression are due to the GH deficiency ensuing from the hypothyroid state. Failure of the GH treatment to increase plasma IGF-I indicates that the feedback regulation on GHRH neurons is operated by circulating GH and/or perhaps tissue but not plasma IGF-I concentrations. Presence of low plasma IGF-I concentrations would be directly related to thyroid hormone deficiency.
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PMID:Hypothalamic-pituitary somatotropic function in prepubertal hypothyroid rats: effect of growth hormone replacement therapy. 167 66

Hormonal feedback regulation of hypothalamic peptides putatively involved in growth hormone (GH) regulation has been studied by measurement of steady-state mRNA levels in male hypophysectomized rats with or without thyroid hormone, corticosterone, testosterone or GH replacement. Hypothalamic GH-releasing factor (GRF) mRNA levels increased progressively following hypophysectomy to 420% of sham levels after 15 days while hypothalamic insulin-like growth factor I (IGF-I) and insulin-like growth factor II (IGF-II) mRNA levels decreased to less than 40% of sham levels. Whole hypothalamic somatostatin mRNA levels were not significantly different from sham. One week of continuous GH infusion restored hypothalamic IGF-I mRNA to levels (95%) indistinguishable from those in sham-operated controls but had no effect on either IGF-II or GRF mRNA. Thyroid hormone, corticosterone and testosterone treatment without GH had no effect on the hypophysectomy-induced reduction of either IGF-I or IGF-II mRNA levels but reversed the elevation of GRF mRNA. We conclude that hypothalamic IGF-I may be involved in GH feedback regulation and thus may function as a hypothalamic modulator of GH. In contrast, IGF-II may be regulated by one of the pituitary trophic hormones but not by GH or the target hormones tested. Finally, hypothalamic GRF mRNA regulation appears to be complex and may include target hormone feedback.
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PMID:Hormonal regulation of rat hypothalamic neuropeptide mRNAs: effect of hypophysectomy and hormone replacement on growth-hormone-releasing factor, somatostatin and the insulin-like growth factors. 167 82

To determine the effect of thyroid status on proTRH-derived peptide processing and secretion, the content and release of TRH and prepro-TRH25-50 (PYE27), as well as somatostatin (SRIF) from median eminence (ME) or olfactory lobe (OL) tissue was studied in the rat. In hypothyroid animals treated by thyroidectomy (Tx), the ME content of TRH and PYE27 was reduced by more than 50%; further, when compared with euthyroid controls there was a significant 2-fold enhancement of the in vitro release of these peptides from ME fragments in response to depolarizing concentrations (60 mM) of potassium. Hyperthyroidism (T4 treatment) caused either no change or an increase in the ME content of these peptides and their response to K+ in vitro did not differ from control animals. The OL content of TRH and PYE27 was unaffected by thyroid status. SRIF levels in both ME and OL as well as in vitro secretion from the ME did not change with either Tx or T4 treatment. The ratio of TRH/PYE27 secretion throughout release and content studies remained stable at 3:1 to 4:1. These findings support the view that TRH in the hypothalamus but not OL is regulated by thyroid hormone. In this location hypothyroidism enhances not only pro TRH synthesis but also release of TRH and another proTRH-derived peptide. The consistent ratio of TRH/PYE27 suggests that regulation of TRH production by thyroid hormone occurs predominantly at the transcriptional level and not through posttranslation processing.
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PMID:Hypothyroidism reduces content and increases in vitro release of pro-thyrotropin-releasing hormone peptides from the median eminence. 167 96

An injection of ovine growth hormone, porcine follicle stimulating hormone, and bovine thyrotropin stimulating hormone increased in Tilapia nilotica plasma concentrations of thyroxine (T4) and reverse triiodothyronine (rT3) after 4 and 8 hr, whereas plasma concentrations of T3 were unaffected. An injection of somatostatin (SRIF) alone did not influence thyroid hormone levels. If, however, SRIF was injected together with these hormones, which raised plasma T4, or together with T4 itself, an increase in plasma concentrations of T3 could be observed, whereas the increase in rT3 was less pronounced. It is concluded that SRIF may change the normal 5-deiodinase (5-D) activity and increased rT3 during hyperthyroxinemia into a 5'-D activity and a rise in T3, respectively, in T. nilotica.
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PMID:Somatostatin increases plasma T3 concentrations in Tilapia nilotica in the presence of increased plasma T4 levels. 167 27

TSH as well as alpha-subunit, secretion has been shown to decrease after the administration of the somatostatin analog octreotide acetate (SMS 201-995). We have studied a 59-yr-old, male patient with a TSH- and gonadotropin-secreting tumor who, because of severe cardiomyopathy, was treated with long-term somatostatin analog rather than surgical resection of the pituitary tumor. Thirteen weeks of treatment with thrice daily sc injection of 100 micrograms octreotide acetate resulted in decreased TSH and alpha-subunit secretion, normal serum thyroid hormone levels, reduction in LH and testosterone level, and significant tumor size reduction. Long-term treatment for 51 weeks has not been associated with any significant side effects. We have shown that octreotide acetate may be a therapeutically valuable modality for certain patients with neoplastic inappropriate secretion of TSH (NIST). A probable effect of octreotide acetate on neoplastic gonadotropes, as evidenced by the reduction of the LH level with a concomitant decrease in testosterone level, is, likewise, suggested.
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PMID:Reduction in size of a thyrotropin- and gonadotropin-secreting pituitary adenoma treated with octreotide acetate (somatostatin analog). 174 May 6

It has been demonstrated that nerve fibres storing immunoreactivity of vasoactive intestinal polypeptide, peptide histidine iso-leucine, neuropeptide Y, substance P, calcitonin gene-related peptide, galanin, and cholecystokinin exists in the thyroid, though the content of these neuropeptides is lower in the thyroid than in other organs, like in the gut. Furthermore, the parafollicular C-cells have been shown to harbour several different peptides: calcitonin, somatostatin, calcitonin gene-related peptide, gastrin-releasing peptide, katacalcin and helodermin. In addition, other regulatory peptides like atrial natriuretic hormone, growth factors, and cytokines are also produced in the thyroid. This review summarizes today's knowledge on the effects of these peptides on thyroid hormone secretion and their possible role in thyroid physiology. So far, functional studies have failed to establish any convincing effect of substance P, calcitonin gene-related peptide, galanin and cholecystokinin on basal or TSH-stimulated thyroid hormone secretion. In contrast, vasoactive intestinal peptide has convincingly been demonstrated to stimulate thyroid hormone secretion, and neuropeptide Y to potentiate the inhibitory action of noradrenaline on TSH-induced thyroid hormone secretion. This suggests that these two neuropeptides are involved in the intrathyroidal neural regulation of thyroid function. Moreover, the C-cell peptides somatostatin, calcitonin, calcitonin gene-related peptide, and katacalcin seem to be involved as inhibitors of thyroid hormone secretion, whereas both gastrin-releasing peptide and helodermin stimulate thyroid hormone secretion. Atrial natriuretic hormone and growth factors, and cytokines seem to inhibit thyroid hormone secretion. Hence, studies undertaken so far suggest a local intrathyroidal peptidergic regulatory concept, the exact role of which remains to be established.
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PMID:Regulatory peptides in the thyroid gland--a review on their localization and function. 182 1


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