UNIPROT:P61278 - FACTA Search

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 synthesis of the cytoskeletal protein actin exhibits, in the rat hypothalamus, a diurnal variation with maxima during morning hours. The objective of the present study was to assess whether melatonin injection could affect the in vitro incorporation of 35S-methionine into actin, as well as the levels of actin mRNA, in the hypothalamus of adult male rats treated either acutely or chronically with the hormone at 10:00 or 18:00. Injection of 100 micrograms/kg of melatonin for ten days at either time induced a significant depression in the incorporation of 35S-methionine into a 43 kDa protein with the electrophoretic mobility of actin. The specific activity of total soluble proteins after labeled methionine incubations decreased only after evening melatonin administration (100 micrograms/kg, ten days). Hypothalamic actin mRNA levels, quantitated by dot-blot analysis, decreased only after the injection of 100 micrograms/kg melatonin for ten days at 10:00. Neither a 10-micrograms/kg dose of melatonin, nor a single injection of 100 micrograms/kg melatonin, caused any significant change in the parameters examined. Melatonin (100 micrograms/kg for ten days) did not modify hypothalamic somatostatin or H-Ras mRNA concentration. These results suggest the existence of an inhibitory effect of melatonin on hypothalamic actin synthesis.
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PMID:Time-dependent effect of melatonin on actin mRNA levels and incorporation of 35S-methionine into actin and proteins by the rat hypothalamus. 197 1

The biorhythm of melatonin in human newborns is established later than that of either serotonin or N-acetylserotonin. Towards the end of the first year of life, the melatonin rhythm is a well established phenomenon and its nocturnal increment is equal to that seen in the pre-school children. Following this period the magnitude of nighttime melatonin increment starts declining and is closely associated with advancing skeletal age. This association between the magnitude of nocturnal increment and skeletal age is also noted in pathological subjects, lower skeletal age with greater magnitude of increment or advanced skeletal age with less increment. Although no inverse relationship between plasma melatonin and gonadotropins could be detected in children, there emerged a marked negative association between melatonin and growth hormone. GRF-induced GH stimulation suppressed melatonin in children as well as in adults. Melatonin pretreatment blocked GRF-induced increment of GH in rats. When animals were given either melatonin or growth hormone, one suppressed the other. It is possible that melatonin-induced growth hormone suppression is somatostatin mediated.
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PMID:The pineal gland in relation to growth and development in children. 346 32

The release of immunoreactive somatostatin (SRIF) from explants of rat medial basal hypothalamus, which were maintained in culture for 24 h, was quantitated by a sensitive RIA. Validity of the specific SRIF assay has been previously established by chromatographic criteria using gel and high pressure systems and by the demonstration of immunological parallelism. After 24 h of culture in medium containing heat-inactivated fetal calf serum, hypothalamic fragments were incubated in serum-free medium, and the release of immunoreactive SRIF was quantitated. Melatonin at concentrations of 10(--8) and 10(--7) M stimulated SRIF release, and no significant increases were observed at concentrations of 10(--9) M or less or at concentrations of 10(--6) M or greater. Serotonin oxalate at concentrations of 10(--8)--10(--5) M significantly inhibited SRIF release. The serotonin antagonist cyproheptadine at a concentration of 10(--5)M had no effect on basal SRIF release but abolished the inhibitory effect of 10(--7) M serotonin. Finally, when hypothalami were incubated with melatonin and serotonin, each at 10(--7) M, SRIF release was unchanged compared to control values. The results suggest that the brain indoleamines, melatonin and serotonin, may modulate GH secretion by effects on SRIF release at a hypothalamic level.
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PMID:Somatostatin release from rat hypothalamus in vitro: effects of melatonin and serotonin. 611 52

Since melatonin (N-acetyl-5-methoxytryptamine) decreases locomotor activity and rearing and increases grooming behavior in a similar manner as somatostatin (SRIF), we examined if melatonin could induce these changes through somatostatinergic neurotransmission in the rat frontoparietal cortex. Male Wistar rats (200-250 g) received a single injection of melatonin (25 microg/kg per day) subcutaneously (s.c.) and were sacrificed 5 hr later. Melatonin treatment increased the number of 125I-Tyr11-SRIF receptors in frontoparietal cortical membranes without any changes in the dissociation constant (Kd). The capacity of SRIF to inhibit basal and forskolin (FK)-stimulated adenylyl cyclase (AC) activity was increased in melatonin-treated rats as compared to the control animals. Melatonin administration also induced a lower AC activity, both under basal conditions and after stimulation of the enzyme via stimulatory guanine nucleotide-binding proteins (Gs), or directly with FK. Functional inhibitory guanine nucleotide-binding protein (Gi) activity was increased in frontoparietal cortical membranes from melatonin-treated rats when compared to controls. Western blot analyzes showed that melatonin administration did not alter the amount of the Gialpha1, or Gialpha3 subunits, but reduced Gialpha2 levels in frontoparietal cortical membranes. No significant changes in SRIF-like immunoreactivity content and SRIF mRNA levels were detected in this brain area after melatonin treatment. Administration of the melatonin receptor antagonist luzindole (10 mg/kg, s.c.) 30 min before melatonin injection did not change the melatonin-induced effects on the SRIF receptor effector system. In conclusion, the present results show that acute melatonin administration increases the activity of the SRIF receptor effector system and decreases Gialpha2 levels in the rat frontoparietal cortex. In addition, the coupling of Gs to AC is disturbed by melatonin.
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PMID:Acute modulation of somatostatin receptor function by melatonin in the rat frontoparietal cortex. 1148 4

Melatonin and somatostatin are known to exert similar effects on locomotor activity. We have previously demonstrated that acute melatonin treatment regulates somatostatin receptor function in the rat frontoparietal cortex. However, the effects of subchronic and chronic melatonin treatment on the somatostatin receptor-G protein-adenylyl cyclase system in the rat frontoparietal cortex are unknown. Melatonin was administered subcutaneously at a daily dose of 25 microg/kg for 4 days, 1 wk or 2 wk. Twenty-four hours after the last injection, the animals were sacrificed. Melatonin did not alter the somatostatin-like immunoreactivity content in the frontoparietal cortex from control and melatonin-treated rats during any of the previously indicated periods. Four days of melatonin administration induced both an increase in the number of [(125)I]-Tyr11-somatostatin receptors and a decrease in the affinity of somatostatin for its receptors in frontoparietal cortical membranes. The increased number of somatostatin receptors in the melatonin-treated rats was associated with an increased capacity of somatostatin to inhibit basal and forskolin-stimulated adenylyl cyclase activity. Melatonin administration for 4 days induced a higher adenylyl cyclase activity both under basal conditions and after direct stimulation of the enzyme with forskolin. No significant differences were observed in the function of Gi proteins in the 4-day melatonin-treated rats. Western blot analyses showed that the 4-day melatonin treatment reduced Gialpha(2) levels, without altering the amount of Gialpha(1). These melatonin-induced changes reverted to control values after 7 or 14 days of treatment. Altogether, the present findings suggest that subchronic melatonin treatment modulates the somatostatin receptor/effector system in the rat frontoparietal cortex.
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PMID:Effects of subchronic and chronic melatonin treatment on somatostatin binding and its effects on adenylyl cyclase activity in the rat frontoparietal cortex. 1239 May

Melatonin is known to increase neuronal activity in the hippocampus, an effect contrary to that of somatostatin (somatotropin release-inhibiting factor, SRIF). Thus, the aim of this study was to investigate whether the somatostatinergic system is implicated in the mechanism of action of melatonin in the rat hippocampus. One group of rats was injected a single dose of melatonin [25 microg/kg subcutaneously (s.c.)] or saline containing ethanol (0.5%, s.c.) and killed 5 hr later. Melatonin significantly decreased the SRIF-like immunoreactivity levels and induced a significant decrease in the density of SRIF receptors as well as in the dissociation constant (Kd). SRIF-mediated inhibition of basal and forskolin-stimulated adenylyl cyclase activity was markedly decreased in hippocampal membranes from melatonin-treated rats. The functional activity of Gi proteins was similar in hippocampal membranes from melatonin-treated and control rats. Western blot analyses revealed that melatonin administration did not alter Gialpha1 or Gialpha2 levels. To determine if the changes observed were related to melatonin-induced activation of central melatonin receptors, a melatonin receptor antagonist, luzindole, was administered prior to melatonin injection. Pretreatment with luzindole (10 mg/kg, s.c.) did not alter the melatonin-induced effects on the above-mentioned parameters and luzindole, alone, had no observable effect. The present results demonstrate that melatonin decreases the activity of the SRIF receptor-effector system in the rat hippocampus, an effect which is apparently not mediated by melatonin receptors. As SRIF exerts an opposite effect to that of melatonin on hippocampal neuronal activity, it is possible that the SRIFergic system could be implicated in the mechanism of action of melatonin in the rat.
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PMID:Acutely administered melatonin decreases somatostatin-binding sites and the inhibitory effect of somatostatin on adenylyl cyclase activity in the rat hippocampus. 1496 59

If melatonin or its analogs are to be used therapeutically in humans, their chronic effects on responsiveness of melatonin target cells need to be assessed. We have previously demonstrated that acute melatonin treatment regulates the somatostatinergic system in the rat hippocampus. In the present study, we have investigated the effects of subchronic and chronic daily treatment with melatonin on the somatostatinergic system in the rat hippocampus. Male Wistar rats (200-250 g) were injected with melatonin (25 microg/kg body weight, subcutaneously) daily for 4, 7 or 14 days and sacrificed 24 h after the last injection. Melatonin administration for 4 days induced a decrease in the hippocampal somatostatin (SRIF)-like immunoreactivity content as well as a decrease in the number of SRIF receptors and an increase in their apparent affinity. The decreased number of SRIF receptors in the melatonin (4 days)-treated rats was associated with a decreased capacity of SRIF to inhibit both basal and forskolin-stimulated adenylyl cyclase activity. These melatonin-induced effects reversed to control values after 7 or 14 days of treatment. Hippocampal membranes from control and melatonin-treated rats showed similar Gi and Gs activities. Melatonin treatment altered neither the functional Gi activity nor the Gialpha 1 or Gialpha 2 levels at any of the time periods studied. The present results suggest that chronic exposure to melatonin results in a tolerance of the hippocampus to this hormone.
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PMID:Activity of the hippocampal somatostatinergic system following daily administration of melatonin. 1524 33

Melatonin and resistance exercise alone have been shown to increase the levels of growth hormone (GH). The purpose of this study was to determine the effects of ingestion of a single dose of melatonin and heavy resistance exercise on serum GH, somatostatin (SST), and other hormones of the GH/insulin-like growth factor 1 (IGF-1) axis. Physically active males (n = 30) and females (n = 30) were randomly assigned to ingest either a melatonin supplement at 0.5 mg or 5.0 mg, or 1.0 mg of dextrose placebo. After a baseline blood sample, participants ingested the supplement and underwent blood sampling every 15 min for 60 min, at which point they underwent a single bout of resistance exercise with the leg press for 7 sets of 7 reps at 85% 1-RM. After exercise, participants provided additional blood samples every 15 min for a total of 120 min. Serum free GH, SST, IGF-1, IGFBP-1, and IGFBP-3 were determined with ELISA. Data were evaluated as the peak pre- and post-exercise values subtracted from baseline and the delta values analyzed with separate three-way ANOVA (p < 0.05). In males, when compared to placebo, 5.0 mg melatonin caused GH to increase (p = 0.017) and SST to decrease prior to exercise (p = 0.031), whereas both 0.5 and 5.0 mg melatonin were greater than placebo after exercise (p = 0.045) and less than placebo for SST. No significant differences occurred for IGF-1; however, males were shown to have higher levels of IGFBP-1 independent of supplementation (p = 0.004). The 5.0 mg melatonin dose resulted in higher IGFBP-3 in males (p = 0.017). In conclusion, for males 5.0 mg melatonin appears to increase serum GH while concomitantly lowering SST levels; however, when combined with resistance exercise both melatonin doses positively impacts GH levels in a manner not entirely dependent on SST.
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PMID:Effects of a single dose of N-Acetyl-5-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in young males and females. 1795 23

The synergetic use of Somatostatin, Melatonin, Retinoids, Vitamins C, D3, and E, Calcium, sulphated Aminoglucosides, and minimum doses of cyclophosphamide in a 70-year old male patient with inoperable scarcely differentiated oesophageal carcinoma, has provided, from the beginning of treatment in 1995 to the present date, an excellent quality of life, as well as a cure with functional recovery. This paper discusses the rationale and molecular action mechanisms of the treatment which has a differentiating, apoptotic anti-proliferation effect, preserving and enhancing, unlike chemo- and/or radiotherapy, both the trophic and functional capacity of organs and tissues, and immunity and antiblastic homeostasis. This result confirms the efficacy of this biological multiple treatment (MDB); it is also in line with the positive results already published on the use of MDB in low-grade NHL (66) and in stage 3 or 4 lung carcinomas (53). The MDB, with no need for hospitalisation, no toxicity and without in the least reducing working activity, gradually and slowly reduced, and then eliminated the tumour formation. According to the author, reporting this case is useful in order to call for greater interest in the possibilities offered to oncology by the MDB biological and receptor treatment.
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PMID:Complete objective response of oesophageal squamocellular carcinoma to biological treatment. 1985 52

The aim of the present study was to investigate the effect of aging on several parameters related to glucose homeostasis and insulin resistance in pancreas and how melatonin administration could affect these parameters. Pancreas samples were obtained from two types of male mice models: senescence-accelerated prone (SAMP8) and senescence-accelerated-resistant mice (SAMR1). Insulin levels in plasma were increased with aging in both SAMP8 and SAMR1 mice, whereas insulin content in pancreas was decreased with aging in SAMP8 and increased in SAMR1 mice. Expressions of glucagon and GLUT2 messenger RNAs (mRNAs) were increased with aging in SAMP8 mice, and no differences were observed in somatostatin and insulin mRNA expressions. Furthermore, aging decreased also the expressions of Pdx-1, FoxO 1, FoxO 3A and Sirt1 in pancreatic SAMP8 samples. Pdx-1 was decreased in SAMR1 mice, but no differences were observed in the rest of parameters on these mice strains. Treatment with melatonin was able to decrease plasma insulin levels and to increase its pancreatic content in SAMP8 mice. In SAMR1, insulin pancreatic content and plasma levels were decreased. HOMA-IR was decreased with melatonin treatment in both strains of animals. On the other hand, in SAMP8 mice, treatment decreased the expression of glucagon, GLUT2, somatostatin and insulin mRNA. Furthermore, it was also able to increase the expression of Sirt1, Pdx-1 and FoxO 3A. According to these results, aging is associated with significant alterations in the relative expression of pancreatic genes associated to glucose metabolism. This has been especially observed in SAMP8 mice. Melatonin administration was able to improve pancreatic function in old SAMP8 mice and to reduce HOMA-IR improving their insulin physiology and glucose metabolism.
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PMID:Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-accelerated prone male mice (SAMP8). 2241 Dec 59

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