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)

Four tumors consisting of pituitary adenomatous cells (AD) intricated with ganglion cells (GC) were studied. Each case was associated with a different clinical syndrome: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome with no hormonal hypersecretion. (a) In the case with acromegaly, immunoreactive growth hormone (IR-GH) was present in 80% of AD. IR-vasoactive intestinal peptide (VIP) was found in 5%-10% of AD and in few GC. Rare GC and processes showed IR-GH-releasing hormone (GRH), -somatostatin (SRIH), -gonadotropin-releasing hormone and -adrenocorticotropin-releasing hormone. (b) In the case with amenorrhea-galactorrhea, IR-prolactin (PRL) was seen in 90% of AD. IR-PRL and -VIP were present in rare GC. (c) In the case with Cushing's disease, 60% of AD and very few GC contained IR-adrenocorticotropin (ACTH) and beta-lipotropin. Rare GC processes contained IR-SRIH. (d) In the case without pituitary hormone hypersecretion, PRL was localized in rare AD and GC. Pituitary hormone and neuropeptides were never colocalized in the same cells. No case displayed IR-neurophysins or -thyroliberin. Pituitary hormones were localized by ultrastructural immunogold labeling. These findings show that: (i) in three cases, pituitary hormones (PRL and ACTH), and, in one case, VIP could be localized in both adenomatous and ganglion cells; (ii) the pituitary hormone-containing cells in the tumors could be related to the hypersecretory syndromes; (iii) intratumoral IR-VIP and -GRH might be involved in GH and PRL hypersecretion in the cases with acromegaly and amenorrhea-galactorrhea.
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PMID:Immunocytochemistry of four mixed pituitary adenomas and intrasellar gangliocytomas associated with different clinical syndromes: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome. 292 94

Pulsatile growth hormone (GH) secretion was compared in young (5 months), middle-aged (11 months) and old (25-29 months) female Sprague-Dawley rats under nonanesthetized, free-moving conditions. Mean plasma GH levels were 99.1 +/- 9.3 ng/ml in young rats, 56.3 +/- 5.8 ng/ml in middle-aged rats and 49.7 +/- 4.9 ng/ml in old rats (p less than 0.01 for young vs. middle-aged and old rats). In young females, 10 out of 17 rats had GH pulses with peak levels greater than 200 ng/ml, in 6 middle-aged females all GH peaks were below 200 ng/ml, and in old females 13 out of 17 rats showed GH peaks of less than 100 ng/ml. The average peak (amplitude) of GH pulses in the old rats (69.3 +/- 8.3 ng/ml) was lower than in the young rats (130.4 +/- 17.5 ng/ml, p less than 0.01) and somewhat lower than in the middle-aged rats (87.0 +/- 8.9 ng/ml). There was no change in intervals between GH pulses. Pituitary GH content in middle-aged and old females (1,189 +/- 60 and 1,100 +/- 89 micrograms, respectively) was significantly lower (p less than 0.05 and p less than 0.01, respectively) than in young female rats (1,464 +/- 76 micrograms). Somatostatin content in the median eminence of old rats (22.4 +/- 1.9 ng) was significantly lower than in young rats (28.5 +/- 1.6 ng, p less than 0.05). It is concluded that GH secretion is reduced in aging female rats, but unlike in aging male rats the decrease is seen at an earlier age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone secretory patterns in young, middle-aged and old female rats. 362 75

GH secretion is stimulated by hypothalamic GH-releasing factor (GHRH) and inhibited by somatostatin. Since GH induces the production of insulin-like growth factors (IGF) in liver and other tissues, it is of interest to learn whether IGF alters GH release through long loop feedback inhibition. Pituitary adenomas which had been removed from six acromegalic patients were processed for dispersed cell cultures and/or cell membrane preparations. Binding studies using 125I-labeled IGF-I, IGF-II, and insulin revealed specific hormone binding for each ligand to cell membranes derived from four somatotropinomas. A partially purified somatomedin preparation inhibited basal and/or GHRH-stimulated GH release from cultured pituitary cells derived from three of four adenomas; there was no effect of somatomedin in one tumor. In a single tumor, insulin also partially inhibited GHRH-stimulated GH release. Additionally, in one nonadenomatous pituitary removed from a patient with diabetes mellitus, insulin and somatomedin inhibited GHRH-stimulated GH release, and insulin inhibited basal GH secretion. These results indicate that specific cell membrane receptors for somatomedin peptides and insulin may be found on cell membranes from GH-secreting tumors, and that somatomedins and insulin can inhibit GH release in cultured human somatotropinoma cells. Thus, these data suggest that somatomedins may exert feedback inhibition of GH secretion in some patients with acromegaly.
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PMID:Regulation of growth hormone release from cultured human pituitary adenomas by somatomedins and insulin. 388 29

Somatostatin receptors in the rat pituitary gland were characterized by binding analysis with a radioiodinated high affinity somatostatin analogue, 125I-Tyr1[D-Trp8]somatostatin. Receptor binding of this derivative reached equilibrium at 30 min and was maintained at a plateau for at least 60 min. Two L-Trp8- labeled somatostatin analogues. 125I-Tyr1- and [125I-Tyr11]somatostatin, displayed less stable and lower specific uptake and higher nonspecific binding. In contrast to the rapid degradation of the L-Trp8 ligands during binding assay, 125I-Tyr1]D-Trp8]somatostatin retained more than 80% of its binding activity after 90 min of incubation with pituitary particles. Pituitary particles bound 125I-Tyr1]D-Tyr8]somatostatin with high affinity (Ka = 8.6 +/- 1.2 X 10(9) M-1) and capacity of 54.4 +/- 2.6 fmol/mg. These binding sites showed specificity for the native peptide and its active analogues, and other peptide hormones, including angiotensin II, thyrotropin-releasing hormone, vasopressin, oxytocin, substance P, and gonadotropin-releasing hormone, did not inhibit tracer binding. A good correlation was observed between the binding affinities of several somatostatin analogues and their potencies as inhibitors of growth hormone release in rat pituitary cells. These findings emphasize the physiological importance of the pituitary somatostatin receptor in mediating the inhibitory action of the peptide on growth hormone release. The use of Tyr1[d-Trp8]somatostatin as a labeled ligand permits accurate determinations of the binding affinity and concentration of receptors for somatostatin in the normal pituitary gland and provides a basis for further studies of somatostatin receptor regulation and receptor-mediated cellular effects of the tetradecapeptide.
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PMID:Pituitary somatostatin receptors. Characterization by binding with a nondegradable peptide analogue. 612 Jan 62

35 male Sprague-Dawley rats, 18 months old, were injected subcutaneously with the catecholamine precursor, L-dihydroxyphenylalanine (L-dopa) (100 mg/kg, twice daily), or vehicle alone, for 8 days in an attempt to increase the amplitude of growth hormone (GH) pulses in old male rats. 40% of young rats had at least one GH pulse greater than 600 ng/ml, over a 6.5 h sampling period, whereas only 22% of old vehicle-treated rats had pulses of similar amplitude. Treatment of old rats with L-dopa increased the number of animals showing elevated GH pulses to 53%. Young animals had mean GH concentrations of 136.5 +/- 14.0 ng/ml over the 6.5 h sampling period, whereas vehicle-treated old animals had mean GH levels of 95.2 +/- 7.7 ng/ml (p less than 0.05). Treatment of old animals with L-dopa increased mean plasma GH concentrations to 132.9 +/- 11.2 ng/ml (p less than 0.05) which was not significantly different from GH values in young rats. Pituitary GH concentration was less in old than in young rats (301 +/- 27.4 vs. 370 +/- 17.4 micrograms/mg protein, p less than 0.05). L-Dopa increased pituitary GH concentrations in old rats to 318 +/- 32.2 micrograms/mg protein, which was not significantly different from that in either young or old vehicle-treated animals. Hypothalamic somatostatin content in both rostral and caudal areas was lower in old than in young rats (p less than 0.01), and L-dopa had no significant effect on somatostatin content. These data indicate that L-dopa can increase the amplitude of GH pulses and elevate mean plasma GH in old male rats to levels present in young male rats, probably by increasing hypothalamic catecholamines.
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PMID:L-dopa restores amplitude of growth hormone pulses in old male rats to that observed in young male rats. 612 69

The effect of hypocalcemia following parathyroidectomy (PTX) on growth hormone (GH) secretion was investigated in unrestrained, unanesthetized male rats bearing chronically implanted indwelling cannulae. During a 6-hour period, starting at about 10 a.m., control rats with a serum calcium (Ca) value of 8.11 +/- 0.38 mg/dl (mean +/- SEM) 2 weeks after sham-operation showed secretory bursts of GH similar to those observed in conscious intact rats. Under hypocalcemia of 4.88 +/- 0.32 mg/dl 2 weeks after PTX, GH secretory episodes were completely suppressed throughout the study. Plasma prolactin (PRL) levels were also decreased in PTX rats as compared with those of sham-operated rats. Daily food intake and body weight gain as well as serum T4 levels in PTX rats were not different from those of sham-operated and intact rats. Pituitary GH content of PTX rats was significantly lower than that of sham-operated and control rats. Pulsatile GH secretion was partially restored in PTX rats by raising serum Ca to 8.43 +/- 0.27 mg/dl through feeding with high Ca diet containing 7% Ca. Immediately after intravenous injection of antisomatostatin sheep serum, pulsatile GH surges recovered in PTX rats despite hypocalcemia of 4.48 +/- 0.74 mg/dl. The mean plasma 6-hour GH levels were significantly higher than those of normal sheep-serum-treated PTX rats (p less than 0.001). These findings suggest that the episodic release of GH is suppressed in hypocalcemic rats after PTX, at least partially via circulating endogenous somatostatin.
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PMID:Attenuation by hypocalcemia of pulsatile growth hormone secretion in conscious male rats. 613 Apr 87

The effects of streptozotocin-induced diabetes on pituitary growth hormone (GH) content and release from incubated pituitaries were investigated. Male rats were made diabetic by a single injection of streptozotocin (65 mg/kg) and sacrificed by decapitation 15 days later. Pituitary GH concentration was significantly reduced in streptozotocin diabetic rats as compared to that observed in control animals. The amount of GH released from hemipituitaries was also lower in diabetic rats than in controls. Kinetic characteristics of somatostatin (SRIF) inhibition of GH release were not affected by the treatment. These results suggest that the decrease in plasma GH observed by some investigators in streptozotocin diabetic rats is probably due to a deficiency in GH storage and/or synthesis rather than a change in the responsiveness of pituitary GH cells to SRIF.
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PMID:Influence of streptozotocin-induced diabetes on growth hormone secretion in the rat. 613 72

The developmental pattern of hypothalamic and pituitary somatostatin and alpha-melanocyte-stimulating hormone (alpha-MSH) was studied in the rat by radioimmunoassay (RIA). Prenatally hypothalamic somatostatin was low and the first increase in content occurred on day 5 of the postnatal period. Pituitary somatostatin was undetectable prenatally and was first detected on day 6 postnatally. Pituitary somatostatin showed the same development pattern as hypothalamic somatostatin. Whole pituitaries were analyzed from the fetuses and neonates. Analysis of anterior and posterior lobes from adults revealed that all the somatostatin was in the posterior lobe. Therefore, it is believed that the somatostatin found in the glands of the younger animals was in the neural lobe. alpha-MSH was detected in the fetal hypothalamus as early as day 16, with a marked increase occurring on day 19 prenatally and a further increase on day 10 postnatally. Pituitary alpha-MSH content, readily detectable on the first day examined, i.e. day 16 of the fetal period, increased throughout development. The effect of alpha-MSH on the release of growth hormone in vitro from pituitaries of rats of various ages was tested. alpha-MSH had no effect on growth hormone release.
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PMID:Pre- and postnatal developmental changes in hypothalamic and pituitary content of alpha-melanocyte-stimulating hormone and somatostatin in the rat. 614 54

Cysteamine (CSH) administered as a single sc injection to rats produced rapid depletion of cerebrocortical Somatostatin-14 like immunoreactivity (S-14 LI) with a significant 48% reduction occurring within 5 min and maximum (72%) decrease at 4 h. The depletion of S-14 LI was associated with a 1.7 fold increase in Bmax of the cerebrocortical S-14 receptors 5 min after CSH administration and a concomitant but slower increase in the affinity of these receptors [dissociation constant (Kd) being 1.8- and 1.6-fold lower than the control at 30 and 60 min, respectively, post CSH]. Incubation of intact synaptosomes with 1 mM CSH at 37 C in vitro for 60 min also caused a rapid depletion of S-14 LI, but in contrast to the in vivo data, there was no change in the Bmax or Kd of the S-14 receptors for up to 30 min beyond which time a 2.8-fold decrease in the affinity of S-14 receptors was observed. Higher concentrations of CSH (greater than or equal to 10 mM) added during the incubation of synaptosomes in vitro completely abolished the specific binding of these receptors. The pituitary S-14 receptors were studied 30 min after CSH administration and unlike the cerebrocortical S-14 receptors at this time did not exhibit any change in Bmax or affinity. When added at the time of the binding assay CSH (1 mM) was without a direct effect on cerebrocortical as well as pituitary membrane S-14 receptors. Furthermore, addition of CSH at the time of binding assay did not destroy the integrity of [125I-Tyr11]S-14. It is concluded that administration of CSH to rats in vivo depletes brain S-14 LI and up-regulates synaptosomal S-14 receptors. Exposure of synaptosomes to CSH in vitro for 30 min also depletes S-14 LI but has no effect on S-14 receptors suggesting that S-14 receptor regulation by S-14 is an in vivo phenomenon or requires the intact cell. CSH has a direct inhibitory effect on S-14 receptor binding after prolonged in vitro incubation. Pituitary S-14 receptors unlike those in the brain are unaffected by S-14 LI depletion at least acutely.
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PMID:Cysteamine-induced depletion of brain somatostatin is associated with up-regulation of cerebrocortical somatostatin receptors. 614 17

Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE- and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species.
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PMID:Effects of synthetic mammalian thyrotrophin releasing hormone, somatostatin and dopamine on the secretion of prolactin and growth hormone from amphibian and reptilian pituitary glands incubated in vitro. 614 54


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