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 administration of monosodium-L-glutamate (MSG) during the neonatal period is known to result in central nervous system lesions in the arcuate nucleus of the hypothalamus and the retina. Rodents so treated exhibit behavioral deficts and endocrinopathies including obesity, hypogonadism, hypothyroidism, pituitary atrophy, tail automutilation and diminished locomotor activity. Assessment of endocrine status revealed normal serum levels of glucagon, thyroid-stimulating hormone and luteinizing hormone, and diminished levels of thyroid hormones and growth hormone in MSG-treated rats. Prolactin levels were elevated in the glutamate-treated male rats. Within the brain hypothalamic levels of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and somatostatin were unchanged. Measurement of neurotransmitters and neurotransmitter-related enzymes in individual hypothalamic nuclei derived from MSG-treated rats revealed normal levels of norepinephrine, serotonin and glutamic acid decarboxylase, but reduced levels of choline acetyltransferase and dopamine in the arcuate nucleus and median eminence. Histochemical methods for visualization of dopamine and acetylcholinesterase in the mediobasal hypothalamus confirmed these findings. The MSG-treated animals exhibited a normal diurnal rhythm of pineal serotonin N-acetyltransferase activity. These data indicate that the MSG-induced endocrine deficiency syndrome results at least partly from destruction of cholinergic and dopamingeric tuberoinfundibular systems in the hypothalamus.
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PMID:Models of neuroendocrine regulation: use of monosodium glutamate as an investigational tool. 3 35

Six children with human growth hormone (hGH) deficiency became hypothyroid during the course of their therapy with hGH. This was accompanied by a decreasing growth rate, clinical symptoms of hypothyroidism and decreased serum T4 concentrations. Three of the 6 patients returned to the euthyroid state, both clinically and biochemically, with cessation of hGH therapy, and reinstitution of hGH precipitated hypothyroidism again in 2 of the three. The patients who remained hypothyroid have evidence of multiple pituitary trophic hormone deficiencies while those who reverted to euthyroidism appear to have isolated hGH deficiency. Evaluation of thyroid function while on hGH showed low T4, free T4 and T3 concentrations. The serum thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) was absent or markedly blunted in 4 of 6 patients while receiving long-term hGH therapy but was normal or exaggerated in all patients when tested before or after only 5 days of hGH therapy. These data indicate that exogenous hGH results in an inhibition of the TSH response to TRH. The mechanism of this inhibition is unclear, but we postulate that it may be mediated by somatostatin secretion in response to pulse doses of hGH.
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PMID:Reversible hypothyroidism in growth hormone-deficient children treated with human growth hormone. 16 11

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.
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PMID:Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects. 40 75

Somatostatin, a growth hormone inhibiting factor (GHIF), was infused into 8 patients with primary hypothyroidism at a dosage of 1000 mug for 105 min. GHIF caused a suppression of TSH levels from 42.6 to 76.9% of preinfusion levels with a mean nadir of 65.0 +/- 4.0%;(mean +/- SEM).
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PMID:The effect of somatostatin on TSH levels in patients with primary hypothyroidism. 120 95

Two studies were performed to determine the importance of endogenous somatostatin (SS) in regulating human TSH secretion. In the first, healthy adult males were studied in random order on two occasions a week apart. They were infused with either saline to maintain euglycaemia, or 10% dextrose to raise blood glucose concentration by at least 3 mmol/L within 10 minutes, and cause hypothalamic SS release. Fifteen minutes after the infusions were commenced, 200 micrograms of TRH was injected intravenously and TSH release was followed for the next 75 minutes. In the second study, persons with elevations of TSH to between 3 and 12 mU/L were also infused with either saline or 10% dextrose. Infusions were continued for 1 hour and the TSH secreted was measured over this time period. There was no significant difference between the euglycaemic or hyperglycaemic studies in TRH-induced TSH secretion, either as areas under the curve, or as mean values at individual times. Mean TSH peaks were seen in both groups at 25 minutes post-TRH. Mean peak values were 8.11 +/- 0.97 mU/L (mean +/- SEM) in the euglycaemic group, and 7.94 +/- 1.18 mU/L in the hyperglycaemic group. Mean area under the curve was 396.3 +/- 53.2 mU/L/75 mins (SEM) for the euglycaemic study and 385.1 +/- 59.5 mU/L/75 mins (SEM) for the hyperglycaemic group. In the infusion study in the persons with mild hypothyroidism, there was no difference in TSH concentration between the two infusion regimes. These results show that in acute studies, hyperglycaemia does not inhibit human TSH release, despite the likelihood of hypothalamic-pituitary SS concentration being increased.
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PMID:The effect of endogenous somatostatin upon human thyrotrophin (TSH) secretion. 134 94

Thyrotropin releasing hormone (TRH) does not promote GH secretion in normal subjects but it stimulates GH in a proportion of hypothyroid patients. In this study the response of GH to thyrotropin releasing hormone (TRH) was evaluated in 21 patients with primary hypothyroidism of different origin: 12 with autoimmune thyroiditis, 3 idiopathic, 3 congenital, 3 iatrogenic. 11 of these patients had never been treated, the others were tested after a drug-free period of at least two weeks. Basal plasma concentration of GH was normal in all patients; after TRH administration, a significant increase in plasma GH was observed in 4 patients. In these responsive patients, somatostatin infusion inhibited the abnormal GH response to TRH. It is suggested that the abnormal GH response to TRH in primary hypothyroidism might be caused by a relative deficiency of somatostatinergic control, which is corrected by exogenous somatostatin administration.
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PMID:Inhibitory effect of somatostatin on abnormal GH response to TRH in primary hypothyroidism. 135 54

Growth hormone (GH)-releasing hormone (GRH) is a stimulatory hypothalamic hypophysiotropic hormone which, along with an inhibitory peptide, somatostatin (SRIF), regulates the synthesis and secretion of GH in anterior pituitary somatotrophs. Although GHRH genes in several species have been characterized, there is only a limited understanding of the neural and hormonal mechanisms regulating GRH biosynthesis and secretion. Recent progress in PCR and in situ hybridization techniques as well as hGRF-transgenic animal models have provided an opportunity to study the regulation of GRH gene expression and secretion as well as its metabolism. The difference in 5'-untranslated sequences in both mouse and rat GRH cDNAs from hypothalamus and placenta has also suggested tissue-specific regulation of the GRH gene. GH excess has been shown to result in a decrease in hypothalamic GRH mRNA as well as GRH content and secretion while GH deficiency caused by hypophysectomy, hypothyroidism or genetic dwarfism causes an increase in GRH mRNA levels as tested by Northern blot analysis or in situ hybridization. Treatment of animals with GH or SRIF inhibits the increased GRH gene expression in the hypothalamic arcuate nucleus. Double immunocytochemistry for hypothalamic GRH and SRIF has shown both axo-perikaryal and axo-axonal connections between GRH- and SRIF- containing neurons. SRIF binding and GH receptor mRNA are demonstrated on a subpopulation of GRH-containing neurons in the hypothalamic arcuate nucleus. It is therefore possible to conclude that regulation of GRH gene expression, primarily related to inhibitory feedback effects of GH and IGFs on hypothalamic GRH gene expression, is mediated at least in part by SRIF or GH. The single transcript of the human GRH gene encodes a 108 amino acid precursor, prepro-hGRH, which is cleaved into the signal peptide and the remaining peptide, pro-hGRH. The latter is further processed to yield two equipotent forms of the releasing hormone, hGRH(1-44)-NH2, hGRH(1-40)-OH, and a carboxyl-terminal peptide (hGCTP) of unknown function. Studies in transgenic mice demonstrate the processing of hGRH-prohormone into both mature forms of hGRH and hGCTP, and provide evidence that hGRH(1-40)-OH is derived from hGRH(1-44)-NH2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Regulation of growth hormone-releasing hormone gene expression and secretion]. 136 Sep 9

The McCune-Albright syndrome, comprising polyostotic fibrous dysplasia, cutaneous pigmentation and endocrine hyperfunction, is occasionally complicated by acromegaly due to a pituitary adenoma. We report a patient with the McCune-Albright syndrome and acromegaly, who developed secondary hypothyroidism and hypoadrenalism, in whom surgical removal of the pituitary tumour was technically difficult. A combination of a long-acting somatostatin analogue ('Sandostatin') and external irradiation were therefore used as treatment.
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PMID:Acromegaly and its treatment in the McCune-Albright syndrome. 142 86

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

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


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