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)

We examined the cell population of somatostatin (SS) in the periventricular nucleus (PN) and growth hormone-releasing factor (GRF) in the arcuate nucleus (ARC) between spontaneous dwarf rats (SDRs; gene symbol: dr), which show isolated GH deficiency, and normal rats using avidin-biotin complex (ABC) immunohistochemistry. The total number of SS perikarya per brain weight in the PN of SDRs was 824.8 +/- 49.6 (mean +/- S.E.M., n = 4), whereas that of controls was 1108.5 +/- 50.1 (n = 4). The GRF perikarya per brain weight in the ARC of SDRs numbered 1281.0 +/- 26.0 (n = 7), as compared to 685.4 +/- 64.6 (n = 7) in the controls. The SS perikarya in the PN of SDRs were significantly reduced (P less than 0.05), while the GRF perikarya in the SDRs were significantly increased (P less than 0.01). These results suggest that GH itself acts on SS to positively regulate its secretion and on GRF in a negative regulatory manner.
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PMID:The cell population of somatostatin and growth hormone-releasing factor using quantitative immunohistochemistry in the isolated GH deficient dwarf rat. 196 67

To clarify the regulatory mechanisms for the secretion of somatostatin (SRIF) from the hypothalamus, the effects of intracerebroventricular (i.c.v.) administration of growth hormone-releasing factor (GRF) and corticotropin-releasing factor (CRF) on SRIF secretion into hypophysial portal blood were examined in pentobarbital-anesthetized male rats. Neither the concentration of SRIF in portal plasma nor the secretion rate of SRIF was changed after i.c.v. administration of 0.9% saline. Administration of 10 ng or 5 micrograms human GRF i.c.v. produced a significant increase in the portal plasma concentration and secretion rate of SRIF. Likewise, 5 micrograms CRF significantly increased the portal plasma concentration and secretion rate of SRIF. These results suggest that the neuropeptides GRF and CRF centrally influence SRIF secretion into hypophysial portal blood.
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PMID:Effects of intracerebroventricular administration of growth hormone-releasing factor and corticotropin-releasing factor on somatostatin secretion into rat hypophysial portal blood. 196 34

To investigate possible sex differences in the feedback regulation of growth hormone (GH) secretion, concentrations of immunoreactive GH-releasing hormone (GRF) and somatostatin (SS) were measured in the median eminence (ME) and the hypothalamus of male and female rats bearing the MtTW15 tumor, which secretes high amounts of GH and prolactin (PRL). Four weeks after tumor implantation in male rats, the GRF concentration in the whole hypothalamus, including the ME, was decreased by 37% (0.29 +/- 0.02 vs. 0.46 +/- 0.02 ng/mg protein in intact male controls; p less than 0.001) and the concentration of SS was increased by 40% (11.5 +/- 0.7 vs. 8.1 +/- 0.3 ng/mg protein in male controls; p less than 0.01). In female rats, the presence of tumor for 4 weeks caused a smaller (18%) reduction in GRF concentrations (0.27 +/- 0.02 vs. 0.33 +/- 0.03 ng/mg protein in intact female controls; p less than 0.05) and no significant change in SS concentrations (10.2 +/- 0.08 vs. 9.7 +/- 0.8 ng/mg protein in female controls). Tumor-related changes in GRF and SS concentrations were also more pronounced in male rats than in females, when determined separately in the microdissected ME and in the remaining hypothalamus. These differences occurred despite similar increases in serum GH, PRL and insulin-like growth factor I concentrations in male and female tumor-bearing rats. To assess which hormone (GH or PRL) was responsible for these changes, intact male rats were treated for 10 days with 2 daily s.c. injections of rat GH (rGH; 100 and 250 micrograms/day), rat PRL (100 and 250 micrograms/day) or vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sexual differentiation of growth hormone feedback effects on hypothalamic growth hormone-releasing hormone and somatostatin. 196 35

The glucose-dependent secretion of the neuropeptides, growth hormone-releasing factor (GRF) and somatostatin (SRIF), by hypothalamic fragments was studied in vitro using a superfusion system. After equilibration of mediobasal hypothalami in HEPES-buffered Krebs-Ringer solution containing 5.5 mM glucose, glucose levels in the superfusion medium were altered. Lowering the glucose concentration in the medium from 5.5 to 2.7 or 1.1 mM provoked a rapid increase in GRF and SRIF release in a concentration and Ca2+-dependent manner. At 1.1 mM glucose, neuropeptide secretion was elevated 3- to 4-fold. The increase of GRF and SRIF release induced by low glucose was transient since stimulated neuropeptide secretion declined to basal levels in the continued presence of low glucose. Furthermore, after reequilibration in 5.5 mM glucose, no second stimulation of neuropeptide release could be induced by reduced glucose. Intracellular glucopenia induced by addition of 2-deoxy-D-glucose (16.5 mM) to the superfusion medium containing 5.5 mM glucose, also evoked increases in GRF and SRIF release. The sensitivity of GRF and SRIF neurons to glucose was absent in the postnatal period until day 9 after birth and then gradually increased. The parallel increases of GRF and SRIF release in response to low glucose observed in the present in vitro study, together with the suppression of plasma GH levels occurring in hypoglycemia in the rat, suggest that, in this condition, the inhibition of GH release induced by elevated SRIF levels predominates whereas the increase of GRF release might serve to attenuate this effect of SRIF.
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PMID:Characterization of the glucose-dependent release of growth hormone-releasing factor and somatostatin from superfused rat hypothalami. 196 36

The effects of a synthetically obtained mixture of amino acids (FACE) were investigated on the trophic and neurosecretory activity of in vitro cultures of fetal rat neuronal cells. The addition of 10(-6) M FACE to the culture medium significantly increased cell DNA content. Secretions of IR-SRIF, IR-VIP, and IR-GRF were also augmented in different proportions by the presence of FACE. Time studies demonstrated that IR-SRIF was significantly increased after 48 (P less than 0.05) and 72 (P less than 0.01) hr of exposure to FACE, and IR-VIP secretion was potentiated after only 24 hr of culture. Dose-response experiments with 10(-7) to 10(-4) M FACE indicated that concentrations of 10(-5) and 10(-4) M significantly increased both somatostatin released to the medium and cell content of IR-SRIF. FACE concentrations as low as 10(-10) M augmented the secretion of IR-GRF, and there was a dose-response correlation between 10(-10) and 10(-5) M FACE. The release and cell content of IR-VIP were also increased by FACE, with a dose-response relation at concentrations of 10(-9) to 10(-6) M. It can thus be concluded that FACE has a powerful effect on the multiplication and survival of fetal cerebrocortical cells and is also an important potentiator of IR-SRIF, IR-VIP, and IR-GRF secretion.
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PMID:Neurosecretory and trophic action on fetal rat neuroblasts induced by an amino acid mixture. 196 52

Steers were actively immunized at 81 days of age against human serum albumin (hSA; controls) or hSA conjugated to either somatostatin (SRIF) or growth hormone-releasing factor (GRF). Binding titres were observed for the respective peptide antigens after all steers had been given booster immunizations. Although no effects of treatment were observed in SRIF-immunized steers, mean serum concentrations of GH and insulin-like growth factor (IGF-I) were suppressed (P less than 0.01) in GRF-immunized steers when compared with hSA-immunized controls. Mean concentrations of prolactin did not differ with treatment but showed seasonal fluctuations (P less than 0.001) associated with changes in the daylength. In contrast to its marked effect upon serum concentrations of IGF-I, immunization against GRF resulted in a relatively small (6%) but significant decrease in body weight gain (P less than 0.01) and an increase in carcass backfat thickness (P less than 0.05). In summary, our findings have shown the susceptibility of steers to growth modulation by GRF immunoneutralization. Secondly, the poor relationship observed between serum concentrations of IGF-I and growth rates in GRF-immunized steers suggested that circulating IGF-I may not be the principle factor determining the post-weaning growth rate in cattle.
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PMID:Growth hormone and insulin-like growth factor-I responses in steers actively immunized against somatostatin or growth hormone-releasing factor. 197 Oct 3

The purpose of these studies was to evaluate the effect of age-related differences in growth rate on the hypothalamic content of growth hormone-releasing factor (GHRH) and somatostatin (SS) and on the short loop feedback regulation of GHRH and SS. Percent weight gain, GHRH content, and SS content in control adolescent (8 weeks) and adult rats (6 months) were compared in normal rats administered supraphysiologic amounts of rat growth hormone (rGH) or in hypophysectomized rats receiving thyroxine and corticosterone with or without physiologic rGH replacement. In control adolescent rats, the rate of weight gain was 5-fold higher than in adult rats. GHRH content was higher in adolescent rats, while SS content was lower. After the administration of supraphysiologic amounts of rGH, GHRH content increased in adolescent rats but did not change in adult rats. SS content was unchanged in either age group. Following hypophysectomy GHRH content declined similarly in both groups, whereas the decrease in SS content was greater in adolescent rats. With replacement rGH, weight gain was restored, GHRH content increased but not fully to control, and SS content did not change. The ratio of SS content to GHRH content (SS/GHRH) was higher in control adult rats than in adolescent rats. SS/GHRH increased following hypophysectomy and returned to control values by rGH replacement. We conclude that age-related differences in growth rate are accompanied by appropriate changes in SS/GHRH and that SS and GHRH are regulated by short loop feedback at both ages with increased responses in adolescent rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of hypophysectomy and growth hormone administration on hypothalamic growth hormone-releasing hormone and somatostatin content: relationship to age-related growth rate. 197 13

Cyproheptadine (CPH)--a putative serotonin antagonist--is known to inhibit growth hormone (GH) response to various pharmacological stimuli, as well as during sleep. To elucidate the possible site at which this drug takes effect, we examined plasma GH and somatostatin response to i.v. GHRH1-44 (1 microgram/kg body wt.) before and after CPH treatment in 10 healthy volunteers. The oral administration of CPH (8-12 mg daily for 5 days; total dose 56 mg) significantly curbed GH response to GHRH as expressed in peak plasma GH values (32.0 +/- 6.1 micrograms/l vs. 12.6 +/- 3.2 micrograms/l; P less than 0.01) and in integrated GH response area (2368 +/- 517 micrograms x l-1 x 2 h vs. 744 +/- 172 micrograms x l-1 x 2 h; P less than 0.01). Plasma somatostatin levels did not change in response to GHRH.
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PMID:The effect of cyproheptadine on plasma growth hormone (GH) and on somatostatin response to GH-releasing hormone in man. 197 4

The adrenergic system is involved in the neural control of GH secretion with both stimulatory and inhibitory influences mainly mediated via GHRH and/or somatostatin modulation. To throw further light on adrenergic neuroregulation of somatotrophic function in man, the effect of various catecholamine agonists and antagonists on basal or GHRH-stimulated GH secretion was studied. Twenty-one adult males aged 20-30 years underwent the following studies: 1. clonidine (CLON), alpha 2-agonist, (15 micrograms/min infused i.v. from 0 to +10 min) alone and preceded by yohimbine (YOH), alpha 2-antagonist, (30 mg orally at -50 min); 2. GHRH (GHRH 44, 1 microgram/kg i.v. bolus at 0 min) alone and preceded by YOH; 3. CLON alone and combined with methoxamine (METHOX), alpha 1-agonist, (1 mg/min infused i.v. from -10 to +10 min); 4. GHRH alone and combined with i.v. infusion of phentolamine (PHEN), alpha 1/alpha 2-antagonist, (0.5 mg/min from -60 to +30 min); 5. GHRH alone and combined with i.v. infusion of salbutamol (SAL), beta 2-agonist, (10 micrograms/min from -5 to +15 min). The GH response to CLON was inhibited by YOH (area under the response curve, mean +/- S.E.: 672.6 +/- 143.0 vs. 219.6 +/- 16.7 micrograms/l/h, P less than 0.05) but was not modified by METHOX (278.4 +/- 94.1 vs. 216.7 +/- 115.5 micrograms/l/h). On the other hand, YOH was unable to affect the GH response to GHRH (339.3 +/- 19.1 vs. 518 +/- 172.8 micrograms/l/h).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of alpha- and beta-adrenergic agonists and antagonists on growth hormone secretion in man. 197 19

We examined the effect of prior exposure to somatostatin (SRIH) on its inhibition of GH and TSH responses to GHRH and TRH stimulation to determine whether SRIH desensitization has physiological significance in man. Six men received GHRH (1 microgram/kg, iv) and TRH (0.3 microgram/kg, iv) 20 min after starting a saline or SRIH (5.5 ng/kg/min, iv) infusion and again 6 h later. Hormone responses were quantified by measuring the area under the curve, corrected for GH concentration at injection time. Similar results were obtained when GH responses were quantified by measuring the hormone secretory rate using the program Detect. Plasma GH and TSH responses to the two GHRH and TRH injections during saline were similar. However, the effects of prior exposure to SRIH were hormone specific. SRIH blunted GH responses to GHRH at 20 min (1609 +/- 286 micrograms/L.min vs. 451 +/- 224), but did not significantly inhibit the responses 6 h later (1422 +/- 410 micrograms/L.min vs. 1000 +/- 302). In contrast, SRIH inhibition of TSH responses to the two TRH injections was similar (first, 946 +/- 201 micrograms/L.min vs. 700 +/- 148; second, 813 +/- 175 micrograms/L.min vs. 562 +/- 66). We next used these results to study whether the previously reported attenuation of GH responses to repeated GHRH stimulation at 2-h intervals is mediated by SRIH. Eight men received GHRH (1 microgram/kg, iv) 380 min after starting a saline or SRIH (5.5 ng/kg/min, iv) infusion or 90 min after starting a primed (5 mg, iv) infusion of propranolol (80 micrograms/min, iv) and again 2 h later. As in the first protocol, GH responses to GHRH were not inhibited when preceded by a 6-h SRIH infusion. However, the 6-h SRIH infusion resulted in a partial restoration of plasma GH responses to the second GHRH injection (saline infusion: first, 1429 +/- 342 micrograms/L.min; second, 254 +/- 75; SRIH infusion: first, 1042 +/- 247 micrograms/L.min; second, 468 +/- 105). beta-Blockade by propranolol resulted in enhanced GH responses to GHRH, but did not prevent the attenuation of GH responses to the second GHRH injection (first, 1937 +/- 366 micrograms/L.min; second, 614 +/- 99). The desensitization to SRIH inhibition of GH responses to GHRH after a 6-h SRIH infusion provides evidence of physiological consequences of SRIH receptor down-regulation. The impaired GH responses to repeated GHRH stimulation are mediated at least in part by enhanced SRIH secretion, which appears independent of a beta-adrenergic mechanism.
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PMID:Impaired inhibitory effects of somatostatin on growth hormone (GH)-releasing hormone stimulation of GH secretion after short term infusion. 197 20


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