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 time-related changes in the plasma levels of growth hormone, insulin, somatomedin C and thyroxine following immunization against somatostatin, have been examined in sheep. In both the treated and control lambs there was a significant increase (P less than 0.01) in growth hormone levels with time from the start of the study (at three weeks of age) through until 13 weeks of age. This increase was mirrored by increasing somatomedin C (IGF-1) levels (P less than 0.001). Thyroxine levels did not change during the period of the study. Immunization against somatostatin did not produce any significant difference between treatment groups or between sexes in the levels of growth hormone or thyroxine. However, IGF-1 level were significantly increased (P less than 0.01) by the treatment in both sexes. The changes in the levels of insulin were complicated by a marked difference between the control groups; the control females being significantly different (P less than 0.001) from all the other animals.
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PMID:Changes in the levels of growth hormone, insulin, somatomedin C and thyroxine in sheep during immunization against somatostatin. 289 94

The present report illustrates the effectiveness of a long-acting somatostatin analog, SMS 201-995 (Sandostatin), in the chronic treatment of acromegaly. Daily doses of 50-300 micrograms were administered subcutaneously to 37 patients. Gradual dose increments induced a progressive GH decrease accompanied by a parallel reduction in plasma somatomedin C concentrations. There was a concomitant amelioration of clinical signs and symptoms throughout the investigational period. No escape phenomenon or tachyphylaxis was observed. It is concluded that chronic therapy with SMS 201-995 represents a promising medical alternative for the treatment of active acromegaly.
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PMID:Long-term management of acromegaly with sandostatin. 290 Jan 89

Plasma somatostatin (SRIF), growth hormone (GH), somatomedin C (IGF1), osteocalcin (BGP), 1,25-dihydroxyvitamin D (1,25-(OH)2D), calcium and inorganic phosphorus were measured in 10 chronically-catheterized fetal calves and in their dams during the two last months of gestation. Thus fetal life is associated with high levels of GH (1.53 +/- 0.14 nmol.l-1), BGP (64 +/- 4 nmol), Ca (2.90 +/- 0.06 nmol.l-1) compared to the results obtained in the pregnant cows. The first week of postnatal life was associated with a tremendous increase in plasma SRIF concentration (from 36 +/- 5 to 106 +/- 15 pmol.l-1; P less than 0.01). These results agree with an intense bone growth during the end of fetal life in the bovine species. However, IG 1 might not play a major role in the regulation of fetal skeletal growth during this period.
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PMID:Systemic bone growth factors concentrations in calves during the perinatal period. 290 75

To explore the GHRH-GH-somatomedin axis integrity in major depressive disorder, 11 drug-free patients and normal subjects matched for age, sex, ovarian status, and body weight received 1 microgram/kg synthetic human GHRH-44 amide as an iv bolus dose. Compared to the normal subjects, the depressed patients had reduced mean basal serum GH levels [2.2 +/- 0.5 (+/- SE) vs. 1.1 +/- 0.2 ng/mL (micrograms/L); P less than 0.05] and a significant attenuation of the net GH response to GHRH [1346 +/- 499 vs. 217 +/- 46 ng.min/mL (micrograms.min/L); P less than 0.01]. The blunted GH responses occurred in the face of significantly increased plasma somatomedin C (Sm-C) levels [1.1 +/- 0.2 vs. 0.6 +/- 0.1 U/mL; P less than 0.05]. The magnitude of GH responses to GHRH did not differ between men and women and was not significantly correlated with age, body weight, baseline serum GH levels, or plasma Sm-C levels in either individual groups or both groups combined. The increased plasma Sm-C levels in the depressed patients could have resulted from diurnal hypersecretion of GH, and the diminished GH responses to GHRH may reflect normal Sm-C-mediated feedback at the level of the pituitary. The presumed GH hypersecretion may be due to decreased hypothalamic somatostatin release and/or hyperactivity of GHRH-containing neurons. Thus, the pathological process resulting in abnormal GH secretory patterns associated with depression may occur primarily at a suprapituitary site.
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PMID:Growth hormone (GH) response to GH-releasing hormone in depression. 311 57

Acromegaly is caused by GH-secreting pituitary adenomas and, in rare cases, by ectopic production of GRH with resultant hypersecretion of GH. Important systemic manifestations include acral enlargement, swelling, disfigurement, glucose intolerance and diabetes, hypertension, nerve entrapment, arthropathy, and cardiac disease. Tumor-related major manifestations are visual impairment, oculomotor paralysis, and hypopituitarism. Morbidity is substantial, and mortality is increased. Diagnosis should be made as early as possible by measuring plasma GH after an oral glucose load and plasma somatomedin C levels. Assessment of a pituitary lesion is best made by CT scanning in the coronal plane. Therapy is mandatory and consists of surgical removal of the pituitary adenoma (usually by the transsphenoidal route) or of the ectopic source of GRH (carcinoids or islet cell tumors). Adjunctive radiation and/or drug therapy is often necessary if complete surgical ablation of the adenoma is not possible. Radiation therapy can be administered as conventional supervoltage x-ray treatment or in the form of heavy particle beams. Drugs effective in partially lowering GH levels are bromocriptine and (not yet released) somatostatin analogues. Long-term follow-up of treated patients is important to guard against recurrence, progression, or development of hypopituitarism.
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PMID:Acromegaly. 331 99

Acromegaly is a disease with unique clinical manifestations. Its confirmatory diagnosis, however, requires basal and dynamic tests of growth hormone secretion. The measurement of circulating levels of somatomedin C has been a valuable addition to the diagnostic armamentarium. We review the etiology of acromegaly, with particular reference to the different histochemical and ultrastructural forms of somatotropic adenomas and their respective clinical behaviors. Ectopic sources of growth hormone-releasing hormone and of growth hormone itself are now well-recognized, though unusual, causes of acromegaly. The treatment of acromegaly is often problematic and far from uniformly successful. Initial enthusiasm for the results of surgical treatment has now been tempered by reports of increasing rates of recurrence on long-term follow-up. The roles of irradiation and pharmacotherapy are reviewed with particular emphasis on the use of bromocriptine, which has added a new dimension to the control of the somatic and metabolic manifestations of hypersomatotropism. Studies have been done recently using a long-acting somatostatin analog with encouraging results.
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PMID:Acromegaly update--etiology, diagnosis and management. 355 58

We encountered a 33-year-old female patient with a pituitary growth hormone (GH)-secreting macroadenoma. The patient was treated with somatostatin analogue (Octreotide) in combination with bromocriptine for 2 months before a transsphenoidal adenomectomy was carried out. Octreotide (300-800 micrograms/day) in combination with bromocriptine was effective in reducing the size of the adenoma by 36%, but produced only a marginal decrease in serum GH. After the operation, bromocriptine alone (15 mg/day) did not lower the level of GH which was produced by residual adenoma tissue. When octreotide (200 micrograms/day) was resumed along with the bromocriptine one year after the operation, it effectively lowered serum GH for 6 months. Thereafter, octreotide therapy became ineffective with a concomitant rise in serum GH and somatomedin C, which was not accompanied by an increase in tumor size. This was a rare case of acromegaly that showed desensitization to octreotide after long-term treatment.
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PMID:Desensitization to somatostatin analogue (Octreotide) observed in a patient with acromegaly. 762 75

The effects of growth hormone (GH) and somatomedin C (SmC), as well as those of apomorphine, dopamine (DA) agonist, or haloperidol (DA antagonist), upon the size of striatal voltammetric peaks 2 and 5 were investigated. Local intrastriatal injections of GH or SmC were followed by an increase in the height of both peak 2 (corresponding to the oxidation of extracellular dihydrophenylacetic acid, DOPAC, a metabolite of DA) and peak 5 (which may represent the oxidation of striatal extracellular somatostatin, SRIF). Treatment with haloperidol also increased the size of the striatal catechol peak but was responsible for a reduction of the neuropeptidergic signal. By contrast, apomorphine determined a decrease in striatal peak 2 (DOPAC) while increasing the levels of peak 5 (SRIF). The data further support the chemical identification of peak 5 at +800 mV as related to the in vivo oxidation of SRIF; in addition they indicate the presence of a functional relationship between this neuropeptide and the GH and DA systems in the striatum of anaesthetised rats.
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PMID:Functional in vivo interaction between growth hormone and dopamine systems are correlated to changes in striatal somatostatin levels as detected by voltammetry. 810 78

Growth hormone (GH) secretion is markedly blunted in obesity. Reportedly, genetically obese Zucker rats show a reduced GH secretion due to an impaired function of hypothalamic neurons producing the GH-releasing hormone (GHRH). The aim of this work was: (1) to compare the in vitro GH responsiveness to GHRH in genetically obese female versus male Zucker rats and, (2) to evaluate the function of hypothalamic GHRH and somatostatin and of pituitary receptors for these neurohormones as assessed by the effectiveness of GHRH and somatostatin on adenylate cyclase (AC) activity. Baseline GH secretion of pituitaries obtained from male and female obese rats was not different and similar to that present in lean counterparts. Stimulation with 10(-7) M GHRH elicited a significantly lower GH secretion from the pituitaries of obese male rats but induced a similar GH secretion from the pituitaries of lean and obese female rats. In these pituitaries, GH concentration was similar in obese versus lean male and female rats [corrected]. A sex-related difference was also evidenced when plasma concentrations of somatomedin C (IGF-I) were evaluated. Obese male rats had lower IGF-I concentrations than lean counterparts, while this was not the case for obese versus lean female rats. Evaluation of AC activity following GHRH disclosed a lower activation in obese than in lean male rats, whereas in the females the enzyme activation was higher in obese than in lean animals. Conversely, the inhibitory effect of somatostatin on forskolin-stimulated AC was similar in pituitary membranes of obese and lean rats of both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone secretion is differently affected in genetically obese male and female rats. 810 99


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