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)

Acute cold stimulus induces activation of the thyreotropic axis characterized by a rapid increase in plasma thyrotropin (TSH). Since pituitary TSH release is mainly regulated by two hypothalamic hormones: thyrotropin-releasing hormone (TRH) and somatostatin, the aim of this study was to analyse whether changes in the steady state mRNA levels and peptide content of these neurohormones occur under acute cold stimulation in rats. Northern blot analysis of hypothalamic somatostatin mRNA levels after 15, 30, 60 or 180 min of cold exposure revealed a 2.0-fold increase after 15 min at 4 degrees C. This augmentation was followed by a return to control values at 30 min. However, the hypothalamic content of somatostatin was not significantly modified at any cold exposure time. TRH mRNA showed a similar pattern to somatostatin, with a 2.5-fold increase after 15 min at 4 degrees C. In contrast, hypothalamic TRH content was significantly decreased after 15 min cold exposure, returning to control values at 30 min. The increase in mRNA levels was specific for the two hypothalamic hormones, since there was no concomitant variation in GAPDH mRNA used as negative control. These results suggest that the organism is quickly aroused by cold stimulus, triggering rapid activation in transcription of the two neurohormones involved in the regulation of the thyreotrope axis. Since the peptide contents did not show the same pattern, a quantitative change in transcription or in mRNA stability does not appear to be a prerequisite for increased peptide expression, suggesting that somatostatin and TRH gene expressions could be regulated at translational or post-translational steps.
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PMID:Rapid changes in somatostatin and TRH mRNA in whole rat hypothalamus in response to acute cold exposure. 791 75

In the present study, it was observed that somatostatin could significantly protect rat gastric mucosa from injury induced by cold-restraint stress and inhibit the stress induced increase of malonaldehyde (MDA) content. In the gastric mucosa of stress rats, the xanthine oxidase (XO) activity were increased and the glutathione peroxidase (GSH-Px) activity were decreased respectively, while the superoxide dismutase (SOD) activity showed no change. After pretreatment with somatostatin, the decrease of GSH-Px activity was significantly reversed, whereas XO and SOD activities were not significantly affected. The above results show that the protective effect of somatostatin against the stress-induced injury of gastric mucosa may be related to an enhancement of the ability of gastric mucosa to scavenge oxygen-derived free radicals.
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PMID:[Protective effect of somatostatin against stress injury of gastric mucosa may be related to the scavenge of free radicals]. 797 28

1. Fourteen days after hypothyroidism was induced either by propylthiouracil (PTU) treatment or by thyroidectomy, the serum thyrotropin (TSH) responses to morphine (5 or 20 mg/kg bw), ether stress (30 min) and cold exposure (60 min) were compared with those in normal rats. 2. The decrease in serum TSH levels after morphine and ether stress found in the normal rats were abolished or much reduced respectively. 3. The increase in serum TSH in response to cold exposure and the diurnal rhythm of serum TSH (lower level at night) were also absent in the hypothyroid rat. 4. The stimulating effects of low dose of thyrotropin releasing hormone (TRH) and the inhibitory effects of somatostatin and apomorphine were completely abolished, while the stimulating effects of a high dose of TRH were much reduced in the hypothyroid rat. 5. These results indicate that in the hypothyroid rat the effect of a lack of negative feedback action of thyroid hormone predominates, and that hypothalamic factors are probably unimportant in the regulation of TSH secretion.
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PMID:Effect of environmental and hypothalamic factors on thyrotropin secretion in the hypothyroid rat. 809 28

Recently the presence of somatostatin receptors on human renal cell carcinomas has been demonstrated by autoradiographic techniques on surgically removed kidneys. In a prospective study we evaluated, by means of 111In-labelled octreotide scintigraphy, the in vivo tumour imaging in a group of patients with biopsy proven renal cell carcinomas at different tumour stages. Seven patients were studied. In three of them (43%) pathological tracer accumulation was demonstrated. In these patients 20 out of 23 known tumour localizations were clearly visualized. Tracer uptake could be inhibited by prior administration of cold octreotide. We conclude that 111In-octreotide scintigraphy can be used to demonstrate, in vivo, metastatic renal cell carcinoma.
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PMID:Imaging of renal cell cancer with radiolabelled octreotide. 823 31

Radiolabelled somatostatin analogues are of potential value in the imaging of somatostatin receptor-positive tumours. Recently, somatostatin receptors have been demonstrated in the osteoblast precursor cells. In this preliminary study, we evaluated the uptake characteristics of indium-111 octreotide in two benign and two malignant bone tumours. Tracer accumulation was observed in all four cases, and overall lesion to background ratio (mean+/-SD) was 2. 74+/-0.84 and 2.98+/-1.49 at 4 h and 24 h, respectively. There was no clear relationship between 111In-octreotide accumulation and the benign or malignant nature of the tumour. In one patient, tracer uptake was inhibited by unlabelled octreotide administration. These results suggest that 111In-octreotide can be taken up by benign and malignant bone tumours. The inhibition of tumour uptake by treatment with cold octreotide supports the concept that specific uptake mechanisms are responsible for 111In-octreotide deposition by bone tumours.
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PMID:Indium-111 octreotide scintigraphy in patients with bone tumours of the extremities. 875 91

This review focuses on the central regulation of thermoregulatory responses with special attention to the participation of thyrotropin-releasing hormone (TRH) in both autonomous and endocrine responses to a cold environment. Besides a direct projection of TRH neurons from paraventricular nuclei (PVN) to the median eminence, and the subsequent activation of the thyroid axis, there are direct projections from the PVN to the autonomic preganglionic neurons controlling autonomous responses. There projections convey information to peripheral targets involved in thermogenesis through the dorsal vagal complex and the spinal cord, for parasympathetic and sympathetic neurotransmissions respectively. Furthermore, cold exposure increases TRH mRNA levels in the PVN but also in dorsal motor and caudal raphe nuclei, thus providing strong evidence for a functional link between autonomous and neuroendocrine systems involved in thermoregulation. The review also focuses on neuroendocrine regulation of cold-induced TRH/TSH release associated with modifications in somatostatin release, with special reference to the participation of several central neurotransmitters (catecholamines, serotonin or GABA) or the influence of sex steroids.
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PMID:Neuroendocrine and autonomous mechanisms underlying thermoregulation in cold environment. 889 54

Glucose tolerance is determined by both insulin action and insulin-independent effects, or "glucose effectiveness," which includes glucose-mediated stimulation of glucose uptake (Rd) and suppression of hepatic glucose output (HGO). Despite its importance to tolerance, controversy surrounds accurate assessment of glucose effectiveness. Furthermore, the relative contributions of glucose's actions on Rd and HGO under steady state and dynamic conditions are unclear. We performed hyperglycemic clamps and intravenous glucose tolerance tests in eight normal dogs, and assessed glucose effectiveness by two independent methods. During clamps, glucose was raised to three successive 90-min hyperglycemic plateaus by variable labeled glucose infusion rate; glucose effectiveness (GE) was quantified as the slope of the dose-response relationship between steady state glucose and glucose infusion rate (GE[CLAMP(total)]), Rd (GE[CLAMP(uptake)]) or HGO (GE[CLAMP(HGO)]). During intravenous glucose tolerance tests, tritiated glucose (1.2 microCi/kg) was injected with cold glucose (0.3 g/kg); glucose and tracer dynamics were analyzed using a two-compartment model of glucose kinetics to obtain Rd and HGO components of glucose effectiveness. All experiments were performed during somatostatin inhibition of islet secretion, and basal insulin and glucagon replacement. During clamps, Rd rose from basal (2.54+/-0.20) to 3.95+/-0.54, 6.76+/-1.21, and 9.48+/-1.27 mg/min per kg during stepwise hyperglycemia; conversely, HGO declined to 2.06+/-0.17, 1.17+/-0.19, and 0.52+/-0.33 mg/min per kg. Clamp-based glucose effectiveness was 0.0451+/-0.0061, 0.0337+/-0.0060, and 0.0102+/-0.0009 dl/min per kg for GE[CLAMP(total)], GE[CLAMP(uptake)], and GE[CLAMP(HGO)], respectively. Glucose's action on Rd dominated overall glucose effectiveness (72.2+/-3.3% of total), a result virtually identical to that obtained during intravenous glucose tolerance tests (71.6+/-6.1% of total). Both methods yielded similar estimates of glucose effectiveness. These results provide strong support that glucose effectiveness can be reliably estimated, and that glucose-stimulated Rd is the dominant component during both steady state and dynamic conditions.
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PMID:Glucose effectiveness assessed under dynamic and steady state conditions. Comparability of uptake versus production components. 907 26

Small cell lung cancer (SCLC) expresses somatostatin receptors that can be traced with 111In-DTPA-octreotide scintigraphy. Although this technique is currently employed for staging and follow-up of neuroendocrine tumors of the gastrointestinal tract, its role in the clinical work-up of SCLC is at present under discussion. A better imaging contrast is desirable and recent reports suggest that this aim could be achieved by pretreatment with cold octreotide. Here we report on the results of 111In-DTPA-octreotide scintigraphy in 12 SCLC patients carried out before and after octreotide treatment. The patients were treated for 7 days with octreotide 200 micrograms three times a day s.c. Uptake was studied at 5 h with whole body planar and SPET imagings. In all cases studied, pretreatment with octreotide was followed by enhancement of tumor imaging. In one patient a better contrast of the lesions was found at the parenchymal and mediastinal levels as well as at brain level, allowing a clear definition of otherwise questionable metastases. After octreotide treatment, a decrease in background uptake in the subdiaphragmatic area was observed in most cases, allowing a better imaging of liver metastases. The enhancement effect was confirmed by semiquantitative analysis of scintigraphic uptake. Taken together, our results seem to indicate that cold octreotide enhancement can improve 111In-DTPA-octreotide imaging and optimize its clinical role in SCLC.
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PMID:Intensification of 111In-DTPA-octreotide scintigraphy by means of pretreatment with cold octreotide in small cell lung cancer. 923 58

The somatostatin analogue octreotide may be used in the diagnosis of carcinoid and other neuroendocrine tumours. Radionuclide scanning following intravenous injection of 111Indium-labelled octreotide (111In-DTPA-pentetreotide) provides a sensitive, non-invasive method of localising somatostatin-positive tumours. The technique may also be used to identify patients who may respond to 'cold' octreotide therapy and to monitor therapeutic efficacy.
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PMID:Octreotide scanning for carcinoid tumours. 933 23

We studied the sensitivity to a depolarizing stimulus of hypothalamic fragments dissected from cycling female donor rats exposed or not to 30-min stress at 4 degrees C. The neuronal response was estimated in terms of the ability of tissue to release somatostatin when stimulated with 40 mM K+. The data showed no differences in response to K+, regardless of the ovarian cycle of the female donors, whereas tissues dissected from ovariectomized or pregnant rats responded significantly to K+. However, when donors underwent previous cold stress, significant differences were noted at all stages of the cycle, except diestrus-1, compared with control rats. We tested whether GABA and/or neuroactive steroids could be involved in this phenomenon and observed no GABA inhibition of somatostatin release in vitro, but inhibition occurred in the presence of a neuroactive steroid, THDOC. The effect of GABA in vivo on somatostatin release was estrogen dependent because bicuculline modified the total amount of somatostatin secreted in estrus but not in diestrus II. Finally, in hypothalamic primary cultures, GABA inhibition of somatostatin release was only detected when steroids were present in the media throughout culture. Our results suggest that steroid-GABA-somatostatin interactions could explain the different responses of neurons to depolarization.
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PMID:Responsiveness to depolarization of hypothalamic neurons secreting somatostatin under stress and estrous cycle conditions: involvement of GABAergic and steroidal interactions. 940 19


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