Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Somatostatin (SS) inhibits in a dose-dependent manner electrically evoked contractions in the rat vas deferens. This action was not modified by yohimbine, naloxone or a mixture of antagonists containing atropine, phentolamine, methysergide, burimamide, propranolol and indomethacin, but was markedly potentiated by reducing the Ca2+ concentration of the medium from 2.5 to 1.25 mM and greatly inhibited when increasing the Ca2+ concentration of the medium from 2.5 to 5.0 mM. Clonidine (CLO), but not beta-endorphin (ENDO) was affected similarly to SS by changing the Ca2+ concentration of the medium. The contractile effect of norepinephrine in unstimulated rat vas deferens was not altered by SS. These results were taken as an indication that SS produces its inhibitory action in the rat vas deferens by interacting with specific SS and its receptors presumably located in the cell membranes of adrenergic nerve terminals. The interaction between SS and its receptors may provoke a decreased diffusion of Ca2+ ions into the nerve terminals and/or a decreased mobilisation of Ca2+ ions from intraneuronal stores thus leading to a reduction in electrically evoked release of norepinephrine.
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PMID:Studies on the inhibitory action of somatostatin in the electrically stimulated rat vas deferens. 46 93

Oxytocin (OT) infusion in normal dogs increases plasma insulin and glucagon levels and increases rates of glucose production and uptake. The purpose of this study was to determine whether the effects of OT on glucose metabolism were direct or indirect. The studies were carried out in normal, unanesthetized dogs in which OT infusion was superimposed on infusion of either somatostatin, which suppresses insulin and glucagon secretion, or clonidine, which suppresses insulin secretion only. Infusion of 0.2 microgram/kg/min of somatostatin suppressed basal levels of plasma insulin and glucagon and inhibited the OT-induced rise of these hormones by about 60-80% of that seen with OT alone. The rates of glucose production and uptake by tissues, measured with [6-3H] glucose, were significantly lower than those seen with OT alone, and the rise in glucose clearance was completely inhibited. Clonidine (30 micrograms/kg, sc), given along with an insulin infusion to replace basal levels of insulin, completely prevented the OT-induced rise in plasma insulin and markedly reduced the glucose uptake seen with OT alone, but did not reduce the usual increase in plasma glucose and glucagon levels or glucose production. To determine whether the OT-induced rise in plasma insulin was in response to the concomitant increase in plasma glucose, similar plasma glucose levels were established in normal dogs by a continuous infusion of glucose and an OT infusion was superimposed. OT did not raise plasma glucose levels further, but plasma insulin levels were increased, indicating that OT can stimulate insulin secretion independently of the plasma glucose changes. Studies by others have shown that the addition of OT to pancreatic islets or intact pancreas can stimulate insulin and glucagon secretion, indicating a direct effect. Our studies agree with that and suggest that in vivo, OT raises plasma insulin levels, at least in part, through a direct action on the pancreas. These studies also show that OT increases glucose production by increasing glucagon secretion and, in addition, a direct effect of OT on glucose production is likely. The OT-induced increase in glucose uptake is mediated largely by increased insulin secretion.
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PMID:Role of insulin and glucagon in oxytocin effects on glucose metabolism. 134 36

Glucocorticoids are thought to inhibit growth hormone (GH) secretion through an enhancement of endogenous somatostatin tone. The aim of our study was to evaluate the effects of GH-releasing hormone (GHRH) and clonidine, an alpha-2-adrenergic agonist which increases GH secretion acting at the hypothalamic level with an unknown mechanism, on GH secretion in seven adult patients (3M, 4F) with non endocrine diseases and on daily immunosuppressive glucocorticoid therapy. Eleven normal subjects (7M, 4F) served as controls. Steroid-treated patients showed a blunted GH response to GHRH (GH peak 8.3 +/- 3 micrograms/L) with respect to normal subjects (GH peak 19.3 +/- 2.4 micrograms/L). The GH responses to clonidine were also blunted (p less than 0.05) in steroid-treated patients (GH peak 5.8 +/- 2.8 micrograms/L) with respect to normal subjects (GH peak 17.6 +/- 2.3 micrograms/L). No significant differences between the GH responses to GHRH and clonidine were observed either in steroid-treated or in normal subjects. Clonidine is not able to enhance GH secretion similar to GHRH in patients chronically treated with steroids. It can be hypothesized that clonidine does not elicit GH secretion decreasing hypothalamic somatostatin tone.
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PMID:Comparative effect of clonidine and growth hormone (GH)-releasing hormone on GH secretion in adult patients on chronic glucocorticoid therapy. 139 65

Diarrhea is a common gastrointestinal problem in diabetes, and its prevalence has been underestimated. The cause of diabetic diarrhea is unknown, but it is probably related to gastrointestinal motility disturbances secondary to diabetic autonomic neuropathy. Other causes (especially primary malabsorption syndromes and islet cell tumors) must be excluded. Treatment of diabetic diarrhea is largely symptomatic and only moderately effective. Antidiarrheal agents may ameliorate acute episodes. Broad-spectrum antibiotics and clonidine hydrochloride (Catapres) have had some success in long-term control. Most recently, subcutaneous administration of somatostatin analogues has been shown to be helpful, the main side effects being drowsiness and vomiting.
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PMID:Diabetic diarrhea. An underdiagnosed complication? 160 50

This study examines the effects of a relatively selective alpha 2-adrenoceptor antagonist, 8-(L-piperazinyl)imado-[1,2-alpha] pyrazine (compound A), and the preferential alpha 2-agonist clonidine on blood glucose, glucose tolerance, and plasma insulin levels in the C57BL/6J ob/ob mouse and its lean littermate. While clonidine raised blood glucose levels and impaired glucose tolerance, oral administration of compound A resulted in decreased blood glucose levels, as well as improved glucose tolerance in ob/ob mice. Insulin levels in ob/ob mice treated with clonidine were significantly reduced, while compound A raised insulin levels threefold and blocked the effects of clonidine when co-administered to the same animals. Clonidine-induced hyperglycemia in lean littermates was not accompanied by a decrease in insulin levels, while a small but significant increase in insulin levels was observed by compound A administration. Glycogen synthesis in diaphragm of ob/ob mice was enhanced after oral administration of compound A and was accompanied by an increase in plasma insulin levels. Concomitant treatment with a potent somatostatin analog to inhibit insulin release blocked the effects of the alpha 2-adrenoceptor antagonist, compound A. These observations suggest that the alpha 2-antagonist studied, increased plasma insulin levels with an accompanying reduction in blood glucose and an improvement in glucose tolerance in a genetic model of insulin resistance. Differential sensitivity to alpha 2-agonist in these genetically obese mice, ob/ob, was demonstrated by decreased insulin levels due to clonidine administration.
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PMID:Effects of an alpha 2-adrenoceptor antagonist on glucose tolerance in the genetically obese mouse (C57BL/6J ob/ob). 197 Aug 47

Clonidine, an imidazoline derivative, is an antihypertensive agent which reduces sympathetic tone by acting in the central nervous system to stimulate alpha-2 adrenoceptors. There is evidence that dopamine and norepinephrine modulate the secretion of GH. Stimulation of GH release is a well-known effect of clonidine in man. Obesity is characterized by an impairment of GH release in response to various stimuli. The aim of this work is to study GH release in response to alpha-2 adrenoceptors stimulation by clonidine in obesity. 12 volunteer obese subjects were studied. 10 normal weight subjects, sex and age matched, were controls. The GH responsiveness was tested with a single oral dose of clonidine (0.15 mg). Blood was sampled for GH radioimmunoassay at 0', 30', 60', 90', 120', 150', 180'. Serum GH basal levels were not significant different in obese subjects compared to controls. In obese subjects, no significant changes occurred in blood GH concentration after clonidine. In normal weight controls, instead, a significant increase of GH values was reached at 90' (P less than 0.05) and at 120' (P less than 0.05) after clonidine. The impairment of GH release after clonidine in obese subjects might be in a reduced serotonin release or in a failure of the hypothalamic-pituitary system to stimulate plasma GH caused by a diminished GH releasing factor stimulatory effect or by an excessive endorphin or somatostatin secretion in obesity.
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PMID:Impaired growth hormone response to clonidine in obesity. 324 43

alpha 2-Adrenoceptor agonists and somatostatin (SS) exert opposite effects on the spike discharge of pyramidal and granule cells in the rat hippocampus. We studied whether clonidine, an alpha 2-adrenoceptor agonist, and yohimbine, an alpha 2-adrenoceptor antagonist, can modulate somatostatin-like immunoreactivity (SSLI) levels, binding of 125I-Tyr11-somatostatin (125I-Tyr11-SS) to its specific receptors, SS-inhibited adenylyl cyclase (AC) activity, and the guanine-nucleotide binding regulatory proteins Gi and G(o) in the rat hippocampus. Clonidine (1 mg/kg, intraperitoneally (IP) or yohimbine (5 mg/kg, IP) injected at both 10 and 16 hours before decapitation did not affect SSLI content in the hippocampus. Clonidine administration decreased the number of specific SS receptors and increased the apparent affinity in hippocampal membranes. This change in SS binding was not the result of a direct effect of clonidine on these receptors because no effect in binding was produced by high concentrations of clonidine (10(-5) M) when added in vitro. Pretreatment with yohimbine prevented the clonidine-induced in SS binding. Yohimbine alone produced a significant increase in the number of 125I-Tyr11-SS receptors and a decrease in its apparent affinity. Clonidine decreased the ADP-ribosylation of a 41- and a 39-kDa G-protein by pertussis toxin (PTX), whereas yohimbine had no effect on the PTX-catalyzed ADP-ribosylation. No significant differences were seen for the basal or for the forskolin (FK)-stimulated AC enzyme activities in the control, clonidine- and/or yohimbine-treated groups. Somatostatin caused a significantly lower inhibition in AC activity in hippocampal membranes of clonidine-treated rats, whereas yohimbine led to an opposite effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha-2 adrenoceptors modulate the somatostatinergic system and G protein levels in the rat hippocampus. 776 86

GH secretion is stimulated by the administration of an alpha 2-adrenergic agonist, clonidine, in several species, including man. This action is probably mediated at the level of the hypothalamus, where the drug may act through inhibition of somatostatin (SRIH) and/or stimulation of GH-releasing hormone (GHRH) release. We have investigated the mode and site of action of clonidine in sheep, because it is possible to collect hypophysial portal blood for the simultaneous determination of GHRH and SRIH in this species under conscious unstressed conditions. Clonidine injection (0.3 mg, iv) resulted in a significant, immediate, and short-lasting (30-min) increase in peripheral GH (14.4 +/- 3.1 vs. 4.8 +/- 1.1 ng/ml; P < 0.01) and portal GHRH (2.7 +/- 0.5 vs. 1.0 +/- 0.2 pg/min; P < 0.01) levels. No change in SRIH secretion was recorded during the same period. Next, we tested the effect of clonidine in sheep actively immunized against GHRH or SRIH. The alpha 2-adrenergic agonist did not affect GH secretion in the anti-GHRH group, whereas immunization against SRIH did not modify the GH response. Finally, we observed that clonidine did not influence GH release from cultured ovine pituitary cells. These data suggest that clonidine acts centrally to stimulate hypophysial GH secretion in the sheep and that this effect is mediated through changes in GHRH, but not SRIH, release into hypophysial portal blood.
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PMID:Role of growth hormone (GH)-releasing hormone and somatostatin in the mediation of clonidine-induced GH release in sheep. 790 8

The GH-releasing activity of the alpha 2-adrenergic agonist clonidine has been extensively studied in the rat, but the mechanism(s) by which clonidine stimulates GH release remains controversial. In the present study, we examined the effects of various doses of clonidine on spontaneous pulsatile GH secretion in conscious rats, and tested the hypothesis that the GH-releasing activity of clonidine is mediated primarily by an inhibition of hypothalamic somatostatin (SRIF) release. In the first experiment, free-moving adult male rats were given either saline or various doses of clonidine i.v. (30, 50 and 125 micrograms/kg) at times of spontaneous peaks (1100 h) and troughs (1300 h) in the GH rhythm. Clonidine, at all doses tested, failed to stimulate GH release when administered at the time of a spontaneous peak. In contrast, injection of clonidine at trough times (when SRIF tone is high) consistently augmented plasma GH levels (mean +/- S.E.M. integrated GH release; 30 micrograms/kg, 1843.0 +/- 484.0; 50 micrograms/kg, 1469.0 +/- 490.3; 125 micrograms/kg, 1675.6 +/- 513.4 vs 201.3 +/- 100.1 ng/ml per 45 min in saline-injected controls; p < 0.05 or less). No significant regression was observed between increasing doses of clonidine and GH release. In the second experiment, i.v. administration of 30 micrograms clonidine/kg during a GH trough period, 30 min prior to GH-releasing factor (GRF) challenge, significantly potentiated the GH response to GRF compared with rats given saline (7218.7 +/- 806.6 vs 4206.9 +/- 1068.1 ng/ml per 30 min; p < 0.05). Clonidine treatment, at all doses tested, resulted in hyperglycaemia and behavioural effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for a primary involvement of somatostatin in clonidine-induced growth hormone release in conscious rats. 791 48

The regulation of growth hormone (GH) secretion and GH mRNA content by the dopaminergic agonist, bromocriptine (BRO); the beta-adrenergic agonist; isoproterenol (ISO); the alpha 1-adrenergic agonist, methoxamine (MET); the alpha 2-adrenergic agonist, clonidine (CLON); the serotonergic agonist, quipazine (QUIP); somatostatin (SS) and GH-releasing hormone (GHRH) were studied using cultured ovine anterior pituitary cells. Clonidine and BRO (10(-6) M) inhibited basal and GHRH (10(-10) M)-stimulated GH release. Bromocriptine enhanced GH mRNA content and potentiated the GHRH (10(-8) M)-stimulated content of GH mRNA, while CLON had no effect on GH mRNA. Quipazine had little effect on GH secretion and no effect on GH mRNA content. Methoxamine and ISO (10(-6) M) increased basal secretion of GH and both enhanced GHRH-stimulated GH secretion. Both MET and ISO increased GH mRNA content of cultured ovine pituitary cells. Somatostatin (10(-7) M) inhibited GHRH-stimulated GH secretion and GH mRNA accumulation. These results support the hypothesis that neurotransmitters may regulate or interact to further modulate pituitary hormone release. Moreover, the data indicate that neurotransmitters may not only regulate secretion but also regulate GH mRNA content and thus affect hormone synthesis.
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PMID:Neurotransmitter receptor agonists regulate growth hormone gene expression in cultured ovine pituitary cells. 793 32


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