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)

Specificity of the effect of prostaglandins (PGs) on hormone release by the anterior pituitary gland was studied using cells in primary culture. Growth hormone (GH) release is stimulated by all eight PGs studied, PGE1 and E2 being 1000-fold more potent than the corresponding PGFs. The release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) remains unchanged upon addition of PGEs. While the basal release of thyrotropin (TSH) is only slightly stimulated by concentrations of PGEs above 10(-6)M, an important potentiation of the stimulatory effect of thyrotropin-releasing hormone on TSH release is observed. The release of GH, TSH and LH is stimulated equally well by PGAs and PGBs at concentrations higher than 10(-6)M, 3 X 10(-6)M, and 10(-5)M, respectively. PGFs do not affect the release of any of the measured pituitary hormones at concentrations below 10(-4)M. The stimulation of GH release by PGE2 can be inhibited by the PG antagonist 7-oxa-13-prostynoic acid, a half-maximal inhibition being found at a concentration of 4 X 10(-5)M of the antagonist in the presence of 10(-6)M PGE2. In the presence of somatostatin 10(-8)M, the inhibition of GH release cannot be reversed by PGE2 at concentrations up to 10(-4)M. 8-bromo-cyclic AMP-induced GH release is additive with that produced by PGE2. The present data show that 1) of the five pituitary hormones measured, only GH release is stimulated by prostaglandins at relatively low concentrations, 2) the PGE-induced GH release can be competitively inhibited by 7-oxa-13-prostynoic acid, 3) the inhibition of GH release by somatostatin cannot be reversed by PGE2 and 4) the PGEs increase the responsiveness of the thyrotrophs to TRH.
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PMID:Specificity of the stimulatory effect of prostaglandins on hormone release in rat anterior pituitary cells in culture. 81 70

The state of the blood vessels is normal at the clinical onset of juvenile diabetes. Vascular changes develop slowly and progressively. According to the growth hormone hypothesis, elevated serum growth hormone is one casual factor in the development of diabetic angiopathy. The hypothesis proposes an effect of growth hormone not on blood glucose but directly on blood vessels. This hypothesis is based on serum growth hormone studies and on a controlled clinical trial of the effect of hypophysectomy on small blood vessels. An animal model of large-vessel disease in diabetes is briefly described. There is a large molecule in diabetic serum causing proliferation of aortic myomedial cells in culture. Growth hormone causes a similar proliferation. A short summary is given of the present situation in somatostatin research relating to diabetes mellitus.
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PMID:Growth hormone's role in diabetic microangiopathy. 98 6

Prophylactitc effect of somatostatin (Growth hormone inhibiting hormone) on restraint stress ulcer formation was studied in rats. Rats treated with somatostatin before and during stress had only the fifth part of the ulcers of the untreated animals after 9 hours of immobilisation. Pathophysiologic mechanism for stress ulcer production is as well discussed as the prohibiting effect of somatostatin on ulcer formation. Prophylactic clinical use has to be considered.
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PMID:Inhibition of stress ulcer formation with somatostatin in rats. 99 71

The present concept of growth hormone is not that of an isolated hormone. Growth hormone is closely related to all other parts of system. Chemically, it belongs of to a family of 3 hormones, with prolactin and human placental lactogen. This chemical relationship produces some similar effects. Physiologically, it belongs to a series of hormonal secretions of which the elements are gradually recognized. Above, it is under the control of a releasing factor, still not identified : somatostatin which is an inhibiting factor, tetradecapeptide recently isolated ; below, the majority of the totality of its actions are developped through another hormone, or group of hormones : somatomedine. Present work on this endocrine system suggests new therapeutic prospects.
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PMID:[Current data on growth hormone]. 110 34

Growth hormone-release inhibiting hormone (somatostatin) inhibits the gastric acid response to food in concious cats. We have confirmed that this tetradecapeptide blocks the food stimulated gastrin release. However, the inhibition of gastrin release is delayed relative to that of acid secretion, &howing that the inhibition of food stimulated acid secretion is by primary effect on the acid secretory mechanism. No evidence was found of potentiation of either the gastric acid output or serum concentration of gastric in response to food.
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PMID:The mechanism whereby growth hormone-release inhibiting hormone (somatostatin) inhibits food stimulated gastric acid secretion in the cat. 121 6

Growth hormone and growth factors have been implicated in the pathogenesis of diabetic retinopathy. Hypophysectomy has been proposed as a treatment for proliferative diabetic retinopathy unresolved by panretinal photocoagulation (PPC). SMS 201-995, a long acting somatostatin analogue which slows down growth hormone secretion, may provide a non-invasive therapy for these rare cases. To assess this possibility, we studied the feasibility and efficiency of long-term SMS 201-995 treatment in diabetics. SMS 201-995 was injected subcutaneously with a continuous pump system at a dose of 400 micrograms/d into 4 insulin dependent diabetic patients suffering from proliferative diabetic retinopathy progressing despite a pan-photocoagulation. The mean age of these patients was 29 +/- 3 years and mean disease duration 18 +/- 3 years. Treatment periods lasted from 6 to 20 months (mean 15 months). Mean 24-hour growth hormone levels decreased by 57% after only one month of treatment (7.4 +/- 1.9 mU/l to 3.2 +/- 0.9 mU/l). The decline continued up to the third month. After the sixth month, signs of resistance to the drug were noted. The frequency of 24-hour GH peaks over 10 mU/l followed a parallel pattern. No rebound was observed when the treatment was progressively discontinued. In 2 patients neovascularization stopped. In the other 2 the process regressed. In all treatment had beneficial effects on the retina. Overall visual acuity improved (7.8 +/- 0.8/10e vs 5.5 +/- 0.8/10e). These effects were obtained within 3 to 6 months. Glycosylated haemoglobin levels did not change (8.8 +/- 1.3% to 9.0 +/- 0.8%). Insulin doses decreased 41% (46.5 +/- 1.7 U/d to 27.3 +/- 3.0 U/d). No severe hypoglycaemia occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stabilization of severe proliferative diabetic retinopathy by long-term treatment with SMS 201-995. 129

Growth hormone (GH) secretion is blunted in diabetic rats. In the present experiment we observed that pituitary GH concentrations and the plasma GH response to an exogenous dose of growth hormone-releasing hormone (GHRH) is decreased in streptozotocin-induced diabetic rats (p less than 0.02) with respect to normal rats. In an attempt to determine if increased somatostatin (SRIF) secretion is responsible for the decreased GH secretion, we studied the effect of modulating SRIF tone on the GH response to GHRH in normal and streptozotocin-induced diabetic rats. Rats were pretreated with either normal sheep serum and saline (NSS+SAL), somatostatin antibodies (SRIF-Ab), or pyridostigmine (PD), an acetylcholinesterase inhibitor hypothesized to reduce hypothalamic SRIF secretion. Pretreatment of normal rats with SRIF-Ab or PD resulted in an increased GH response to exogenous GHRH in comparison to NSS+SAL-pretreated normal rats at 5 min postinjection. In contrast, pretreatment of diabetic rats with SRIF-Ab or PD did not alter the GH response to exogenous GHRH when compared to NSS+SAL-pretreated diabetic animals. These results suggest that the blunted GH response to exogenous GHRH observed in streptozotocin-induced diabetic rats may not be due to an increase of endogenous SRIF tone.
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PMID:Hypothalamic regulation of impaired growth hormone secretion in diabetic rats. 1. Studies in streptozotocin-induced diabetic rats. 135 66

In a group of patients affected with psoriatic arthritis the effects of the association between gold salts (GS) and somatostatin (SOM), in comparison with two groups treated with SOM and GS respectively, were investigated. Sixty patients with psoriatic arthritis were selected and randomly allocated in three groups of twenty patients each. Group 1 received SOM infusion (250 micrograms/h for 96 h) and was assessed at baseline and 1, 15, 30, 60, 90 and 120 days after; Group 2 received intramuscular GS and was assessed at baseline, four months later, and then every month for four months; Group 3 received GS for 8 months; at the fourth month SOM was infused (as in Group 1) and the patients assessed at baseline four months later and then as Group 1. Assessment was made with the Ritchie index, pain scale and morning stiffness evaluation. Growth hormone was assayed in Group 1 every 4 h for 24 h the day before and the day after SOM infusion. The association between GS and SOM demonstrated a particular analgesic activity, effective on joint pain and tenderness, that lasted for all four months of follow-up. SOM showed a good response only after 15 and 30 days, and GS proved to be effective at about the sixth month of treatment. Side effects were reported in Group 1 (abdominal cramps, mild erythrodermia and supraventricular arrhythmia). A growth hormone circadian rhythm was found in psoriatic patients both before and after SOM treatment. The beneficial effect of the SOM/GS combination is demonstrated in psoriatic arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gold salts and somatostatin: a new combined analgesic treatment for psoriatic arthritis. 135 20

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

Growth hormone (GH) hypersecretion is well documented in insulin-dependent diabetes mellitus (IDDM). Somatostatin inhibits GH in acromegalics and healthy subjects although data on its inhibitory effects on high GH levels in IDDM patients are controversial. The effect of treatment with the somatostatin analogue octreotide ("Sandostatin") on GH secretion, IGF1 levels and metabolic control was investigated in insulin-dependent diabetics. Growth hormone and blood glucose were measured at hourly intervals whilst IGF-I was measured every 6 hours during the 24-h period before and after 7 days' treatment with octreotide (200 micrograms subcutaneously three times daily) in 10 C-peptide negative diabetics. Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). The shape of 24 h GH profile curve changed significantly on octreotide treatment (p less than 0.05) when it consisted of three nadirs and three peaks closely linked with the time of octreotide administration. Moderate (abdominal discomfort) to severe hypoglycaemia) transient side effects have been observed in all treated patients. The results of this study showed that short-term treatment with octreotide given s. c. every eight hours modulates the pattern of GH secretion in C-peptide negative insulin-dependent patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of the somatostatin analogue octreotide on growth hormone secretion in insulin-dependent diabetics without residual insulin secretion. 151 89


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