UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anterior pituitary gland of the human fetus has the ability of synthetizing, storing and secreting hormones early during gestation. The patterns of plasma concentrations of hGH, ACTH, LH and FSH during gestation indicate a maximum of secretion at mid-gestation followed by a progressive decrease of these concentrations until term. In contrast, the secretions of PRL and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence of releasing factors in the fetal hypothalamus has been established (TRF, LRF, somatostatine) and it was postulated that early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs and, later in development, there was a maturation of inhibitory or restraining influences mediated via the CNS that modulate the secretion of the fetal adenohypophyseal hormones. Observations made with anencephalic newborns confirm that a functional hypothalamus is necessary for the secretions of each of the hormones of the anterior pituitary gland with the exceptiion of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during fetal life, it appears evident that this regulation can only be fully understood with the existence of a GRF (Growth Hormone Releasing Factor).
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PMID:[Hypothalamic factors in the human fetal brain: their role in the ontogeny of fetal hypophyseal functions]. 20 94

Basal serum growth hormone and response of GH to GRF in 10 patients with noninsulin-dependent diabetes and in 10 control subjects were studied. The basal GH level in NIDDM was higher than that in control subjects. There was a significant difference. After an intravenous bolus of hGRF 1-29 NH2 with the dose of 1 microgram/kg body weight, GH (Peak level-basal level) decreased in NIDDM patients in comparing with control group (P < 0.05). These findings may suggest that the pituitary GH reserve is reduced in patients with NIDDM. There exists some defect in central GH control in diabetics with enhanced somatostatin secretion and abnormal sensitivity of the GH secretion cells to a variety of regulatory factors including GRF, glucose, amino-acids, free fat acid.
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PMID:[Blunted growth hormone response to hGRF 1-29 NH2 in patients with non-insulin-dependent diabetes mellitus]. 130 83

Experimental evidence indicates that the neonatal gonadal steroid environment is an important determinant of the sexual dimorphism of GH secretion and body growth. However, the influence of the sex steroids in GH control during adult life and their mechanism/site of action are largely unknown. In the present study we examined the effects of adult gonadectomy (GNX) and short term adult exposure to 17 beta-estradiol (E2) on both spontaneous and GRF-stimulated GH release in free-moving adult male rats. The rate of body weight gain was also monitored. GNX (3 weeks postoperatively) resulted in a 2-fold reduction in GH pulse amplitude compared to that in sham-operated control rats, but did not significantly alter the GH nadir or the interpeak interval. Exposure to E2 (sc implants) for 4 days markedly disrupted the spontaneous GH secretory profile of both sham-operated and GNX rats; E2-treated animals exhibited a striking elevation (4- to 20-fold) of GH trough levels and a significant decrease in GH interpeak interval, remarkably similar to the typical female rat GH secretory profile. The augmentation in both GH nadir and GH pulse frequency was evident as early as 12 h after a single sc injection of E2 valerate. In sham and GNX rats bearing control implants, the GH response to 1 micrograms rat GRF-(1-29)NH2, iv, was significantly greater when GRF was administered at peak (1100 h) than at trough (1300 h) times of GH secretion; the latter is known to be due to antagonism by the cyclical increased release of endogenous somatostatin (SRIF) in the male rat. Treatment with E2 abolished this time-dependent difference in both groups and produced a regular pattern of GH responsiveness to GRF similar to that typically observed in the female rat, thus suggesting that E2 has altered the pattern of hypothalamic SRIF secretion from a cyclic to a more continuous mode of release. Chronic exposure to E2 for 2 weeks resulted in an almost 6-fold inhibition of the rate of body weight gain in sham-operated male rats to levels comparable to those in normal adult female rats. Taken together, these results demonstrate that short term exposure to E2 during adult life can profoundly feminize the male pattern of spontaneous and GRF-stimulated GH secretion, as well as rate of somatic growth.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Short-term adult exposure to estradiol feminizes the male pattern of spontaneous and growth hormone-releasing factor-stimulated growth hormone secretion in the rat. 134 80

The densest distribution of somatostatin (SRIF) neuron perikarya is localized in the hypothalamic periventricular nucleus (Pe) close to the third ventricle, from which many fibers are projected to the median eminence. The release of SRIF in the neurohemal organ into the anterior pituitary modulates GH secretion from pituitary somatotrophs. When SRIF input from the hypothalamus to rat anterior pituitary is reduced by either neurosurgery or SRIF antiserum iv injection, the responsiveness of the pituitaries to human GH releasing factor (hGRF) in an in vitro perifusion system is markedly attenuated. Moreover, SRIF pretreatment facilitates the GH release response of dispersed anterior pituitary cells to hGRF. The long lasting SRIF effect to sensitize somatotrophs appears to take place beyond cAMP formation or as an unknown distal effect. These findings indicate that SRIF neurons in the Pe play a role in maintaining the pituitary responsiveness to GRF in addition to the original action to inhibit GH secretion. Neuronal networks between Pe-SRIF neurons, and intra- and extrahypothalamic nuclei are identified by Pe stimulation test on GRF-GH secretion. In addition to the physiological role in maintaining pituitary responsiveness, Pe SRIF neurons have a wide influence on specific SRIF receptor binding in various brain regions as well as in the anterior pituitary. Shortly after lesioning the Pe neurons, there is a continuous increase in plasma GH level with a transient increase in specific binding of 125I-Tyr 11-SRIF-14 to the anterior pituitary. Furthermore, there is a similar but a little longer increase in binding of the radioligand to some brain areas such as the cerebral cortex, hippocampus, and amygdala nuclei. However, neuronal connections between the SRIF neurons and nuclei which are up-regulated by the lesioning have not been fully proven. When the labeled ligand is infused into the lateral ventricle, it is rapidly and widely distributed in many periventricular structures in the lateral and third ventricles. These findings suggest that SRIF produced in the Pe neurons is transported to other brain areas via cerebrospinal fluid in addition to neuronal connections for modulating the activity of neurons which have SRIF receptors. Thus, hypothalamic Pe SRIF neurons have dualistic roles for controlling anterior pituitary function and modulating CNS neuron activity.
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PMID:[A hypothalamic hormone-somatostatin--from endocrinology to neurophysiology]. 135 33

A 42-year-old woman with a family history of multiple endocrine neoplasia type 1 (MEN 1) presented with symptomatic hypoglycaemia and peptic ulceration. Investigation revealed an insulinoma, hyperparathyroidism, hypercalcitoninaemia with a positive pentagastrin stimulation test, acromegaly due to a GRF-oma, hyperprolactinaemia and normal serum gastrin levels. Five pancreatic tumours were removed at laparotomy and immunostaining was positive for insulin, calcitonin, somatostatin and glucagon. Post-operatively she developed elevated serum gastrin levels and gross peptic ulceration, despite H2-blockers, and died of gastro-intestinal haemorrhage suggesting that removal of the somatostatinoma may have allowed increased gastrin secretion from a gastrinoma. This case emphasizes the importance of measuring a wide variety of tumour marker peptides in MEN 1 and suggests that caution is required in interpretation of the pentagastrin stimulation test in such cases. Patients with MEN 1 and known peptic ulceration may require perioperative omeprazole treatment even if serum gastrin levels are normal.
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PMID:A case of multiple endocrine neoplasia: hyperparathyroidism, insulinoma, GRF-oma, hypercalcitoninaemia and intractable peptic ulceration. 135 65

In order to elucidate whether the gender differences observed in the somatotropic cells of adult rats are mediated by hypothalamic neuropeptides, a morphometric analysis was made of the GH-immunoreactive cells of adult rats treated intraventricularly with colchicine. The morphometric and morphological findings obtained were correlated to the basal serum levels of GH at the time of sacrifice. Treatment with colchicine was seen to increase serum GH levels; this increase was accompanied by an increase in the intensity of the reaction of the GH-cells and, morphometrically, an increase in their size due to an increase in the nuclear area, but with no significant changes in the cytoplasmic area. The results suggest that in the absence of somatostatin and GRF the basal release of GH is elevated in a similar fashion in both sexes, in turn suggesting that gonadal steroids might act at hypothalamic level on the release of somatostatin and, indirectly, on the intracellular pool of GH and hormonal secretion.
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PMID:Morphometric changes in GH-immunoreactive adenohypophyseal cells induced by intraventricular administration of colchicine to adult rats. 136 Aug 49

Immunohistochemical and in situ hybridization localization of peptides derived from, and mRNAs encoding, prepro-somatostatin (ppSS) and prepro-growth hormone-releasing factor (ppGRF) was carried out on hypothalami from rats flown on biosatellites COSMOS 1887 and 2044 to investigate possible effects of reduced gravity on central hypophysiotropic systems controlling growth hormone (GH) secretion. Results from the COSMOS 1887 mission indicated that both SS and GRF immunostaining in the median eminence were diminished in flight animals relative to controls; no differences between groups in staining for other peptidergic neurosecretory systems were apparent. Animals flown on COSMOS 2044 displayed a more pronounced depletion of GRF than SS immunoreactivity from neurosecretory terminals in the median eminence. In addition, flight animals displayed significant 46-50% reductions in the number and signal intensity of presumed hypophysiotropic cells in the arcuate nucleus expressing ppGRF mRNA; positively hybridized cells in the region surrounding the ventromedial nucleus were less markedly affected. Both indexes of ppSS mRNA levels in the anterior periventricular nucleus were similar in flight and control rats. An additional group of animals that experienced hindlimb suspension, a manipulation that mimics the effects of weightlessness on several parameters, did not differ from controls in any of the above measures. These data suggest that exposure to microgravity results in a preferential reduction in GRF peptide and mRNA levels in hypophysiotropic neurons, which may contribute to impaired GH secretion described previously in animals subjected to spaceflight. Effects of weightlessness are not mimicked by hindlimb suspension in this system.
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PMID:Effects of spaceflight on hypothalamic peptide systems controlling pituitary growth hormone dynamics. 152 45

The effects of intravenous (IV) and intracerebroventricular (ICV) administration of either bovine growth hormone releasing hormone (GRF) or thyrotrophin releasing hormone (TRH) on plasma growth hormone (GH) and glucose levels have been examined in sheep. Intravenous GRF 1-29NH2 at 3 and 30 micrograms stimulated an increase in GH levels in a dose-dependent fashion; administration of GRF into a lateral cerebral ventricle, however, produced a smaller GH response which was similar at these two doses. Evaluation of somatostatin levels in petrosal sinus blood (which collects pituitary effluent blood) showed that ICV administration of GRF stimulated a release of somatostatin into the blood. Furthermore, concurrent administration of GRF and a potent anti-somatostatin serum ICV resulted in a much enhanced release of GH which was similar to that obtained with a comparable dose of GRF given IV. TRH (as another putative GH-secretagogue) was also administered both IV and ICV. When given IV, 200 micrograms (but not 100 micrograms) TRH produced an elevation in GH levels. By contrast, when 5 micrograms TRH was given ICV there was a decrease in circulating GH levels, but no change in plasma somatostatin concentrations. These results indicate that the smaller GH response to ICV- compared with IV-administered GRF is due to the release of somatostatin within the brain. In addition, it would seem that TRH is not a physiological GH-secretagogue in sheep.
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PMID:Neuroendocrine regulation of growth hormone secretion in sheep. V. Growth hormone releasing factor and thyrotrophin releasing hormone. 161 57

To examine the effects of anabolic agents given during late gestation on the maternal and fetal somatotropic axes, we injected pregnant ewes twice daily with 0.15 mg somatocrinin (GRF)-(1-29) for 10 days beginning on day 130 of gestation. Maternal and fetal endocrine changes were compared with control animals using both in vivo and in vitro approaches. Treatment with GRF increased maternal plasma levels of growth hormone (GH) and insulin-like growth factor I (IGF-I;P less than 0.05) but not IGF-II. Under in vitro test conditions, maternal pituitary cells showed a greater maximal response (P less than 0.001) to GRF. In the fetuses of treated ewes, cord plasma GH levels were not significantly increased compared with controls. These animals had similar IGF-I but higher IGF-II (P less than 0.05) plasma levels. The maximal response of fetal pituitary cells to GRF was increased (P less than 0.001). GRF treatment had no influence on maternal and fetal pituitary cell responses to somatostatin under either basal or GRF-stimulated conditions. In addition, these treatments did not affect plasma levels of placental lactogen, glucose, or free fatty acids in the maternal and fetal sheep. These data are compatible with the hypothesis that treatment of pregnant ewes in the last days of gestation with GRF could support accelerated fetal growth.
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PMID:GRF treatment of late pregnant ewes alters maternal and fetal somatotropic axis activity. 167 20

A striking sexual dimorphism exists in the pattern of GH secretion and rate of somatic growth; however, the mechanism(s) mediating this sex difference is unknown. To elucidate the physiological roles of the hypothalamic neuropeptides, somatostatin (SRIF) and GRF, and their interrelation, in generating the sexually dimorphic GH secretory pattern we examined: 1) GH responsiveness to exogenous GRF and 2) the effects of immunoneutralization of endogenous SRIF and GRF on GH secretory dynamics, in free-moving male and female rats. In males, the GH response to 1 microgram rat(r)GRF(1-29)NH2 iv was significantly greater at peak compared to trough times of GH secretion (925.2 +/- 250.8 vs. 95.6 +/- 27.8 ng/ml; P less than 0.02), the latter known to be due to antagonization by the cyclic increased release of endogenous SRIF. In contrast, females failed to exhibit a time-dependent difference in GH responsiveness to GRF. Passive immunization with a specific antiserum to SRIF in males resulted in significant elevation of GH nadir levels but had no effect on GH peak amplitude. In contrast, immunoneutralization of endogenous SRIF in females caused a marked augmentation of plasma GH levels at all time points; there was a significant increase in GH peak amplitude (171.3 +/- 39.9 vs. 67.5 +/- 11.3 ng/ml; P less than 0.05), GH nadir (18.3 +/- 2.7 vs. 5.8 +/- 1.1 ng/ml; P less than 0.01) and mean 6-h plasma GH level (78.7 +/- 4.1 vs. 33.1 +/- 5.8 ng/ml; P less than 0.001), compared to normal sheep serum-treated controls. These results indicate that the pattern of hypothalamic SRIF secretion in females does not follow the male-like ultradian rhythm. Passive immunization with a specific antiserum to GRF obliterated spontaneous GH pulses in both sexes. Moreover, in females, anti-GRF serum attenuated GH nadir levels (4.3 +/- 1.7 vs. 21.4 +/- 3.5 ng/ml; P less than 0.01) indicating a physiological role for GRF in maintaining the elevated basal GH level of females, in addition to its important role in generating the episodic GH pulses. Taken together, these findings provide support for the hypothesis that, in female rats, the pattern of hypothalamic SRIF secretion into hypophyseal portal blood is continuous, rather than cyclical, as in the male; whereas in the case of GRF secretion, in addition to steady-state release which occurs at a higher level in females than males, there is also episodic GRF bursting which does not follow a specific rhythm, as in the male.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sexual dimorphism of somatostatin and growth hormone-releasing factor signaling in the control of pulsatile growth hormone secretion in the rat. 167 85

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