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 effect of growth hormone-releasing factor (GRF) 1-44 on growth hormone and somatostatin release in plasma has been studied in 20 obese children. Twenty age and sex-matched children with normal weight served as controls. Mean peak growth hormone response in obese children after 1 microgram/kg body wt. GRF 1-44 was significantly lower than in controls (23.7 +/- 3.6 ng/ml vs. 41.1 +/- 3.0 ng/ml; P less than 0.01), as were mean integrated growth hormone response areas (1544 +/- 272 ng X ml-1 X 2 h vs. 2476 +/- 283 ng X ml-1 X 2 h; P less than 0.01). Mean plasma levels of somatostatin-like immunoreactivity did not change after GRF in both groups. Mean somatomedin-C levels in obese children were significantly higher compared to controls (1.6 +/- 0.4 U/ml vs. 0.86 +/- 0.4 U/ml; P less than 0.01). Somatomedin-C levels were not related to the integrated growth hormone responses. In conclusion there is no relation between somatomedin-C levels and the reduced growth hormone-releasing effect of GRF in obese children. GRF does not alter peripheral somatostatin-like immunoreactivity levels either in normal or obese children.
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PMID:Circulating somatomedin-C levels and the effect of growth hormone-releasing factor on plasma levels of growth hormone and somatostatin-like immunoreactivity in obese children. 288 8

The use of biotechnology now allows adequate supplies of previously scarce substances. This has enabled evaluation of some of these substances as enhancers of animal performance. Growth hormone (GH) shows promise as a stimulator of lactation in a number of species, but its effects on the stimulation of growth are somewhat equivocal. Somatocrinin, by virtue of its GH- releasing activity, may also be potentially useful, though to date the effects of somatocrinin administration have been less promising than those for GH directly. Somatomedin (IGF-1), as the active mediator of GH, might be expected to be useful in growth promotion but, as yet, it has not been convincingly demonstrated to stimulate growth in normal animals. All these hormones have the major drawback that, until a suitable slow-release/delivery mechanism is available, they need to be administered very frequently. An alternative approach, immuno-neutralization of the growth inhibiting effects of somatostatin, has been demonstrated to enhance growth; although at present still requiring multiple treatments such a technique potentially has many advantages.
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PMID:Biotechnology in the potential practical application of somatotrophic hormones for improving animal performance. 288 69

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

A brief introduction is provided to the physiological actions of somatostatin, somatomedins and growth hormone releasing factor (GRF) in relation to human growth hormone (hGH). The development of recombinant DNA techniques allowed the biosynthesis of somatrem (methionyl hGH), and as the methods were refined, authentic recombinant hGH (methionyl-free) has been produced. rhGH is currently undergoing clinical trials in several countries. Recombinant IGF-1 has also been developed by similar methods, utilizing a yeast as the host cell. In contrast, GRF is too small to be biosynthesized, but can be produced by classical peptide synthesis. Only the N-terminal sequence is required for biological activity, and may be 29, 40 or 44 residues long. Research into the biological effects of both IGF-1 and GRF is underway.
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PMID:Current research on recombinant human growth hormone and the related growth factors, IGF-1 and GRF. 310 8

Somatomedin-C stimulates somatostatin release to a maximum of 390 percent of basal release during short-term (20-minute) incubation of rat hypothalamus. It has no effect on basal or stimulated growth hormone release from primary cultures of rat adenohypophyseal cells during a 4-hour incubation, but inhibits stimulated release by more that 90 percent after 24 hours. These findings suggest that somatomedin-C participates in the growth hormone negative feedback loop with an immediate effect on hypothalamic somatostatin and a delayed effect on the anterior pituitary.
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PMID:Somatomedin-C mediates growth hormone negative feedback by effects on both the hypothalamus and the pituitary. 626 17

With regard to diabetic retinopathy, in addition to the demonstration by the DCCT study that prevention is achieved by good metabolic control, our present knowledge on physiopathology leads us to imagine three types of possible therapeutic approach; inhibition of glucotoxicity, improvement of capillary flow, blockade of angiogenesis. 1) Inhibition of glucotoxicity Aldose reductase inhibitors can prevent cataract in diabetic or galactosemic rats. The effect of these drugs on retinopathy, evaluated in some clinical trials, remains controversial, suggesting a minor role. Aminoguanidine is an inhibitor of formation of advanced glycosylation end-products (AGE). This compound has been tested on a model of experimental retinopathy in rats. Parallel to the AGE decrease in retina, formation of microaneurysms and loss of endothelial cells in capillaries were delayed. Clinical tolerance allows human application and randomised trials will give further information on this potentially efficient drug. 2) Improvement of capillary flow This objective can be obtained by drugs inhibiting platelet aggregation or improving erythrocyte or leucocyte deformability. Clinical trials using such compounds were not very conclusive. 3) Blockade of angiogenesis Proliferation of new vessels is a rather severe stage of diabetic retinopathy. Angiogenesis is due to factors locally produced (as FGF, TGF and u-PA produced by anoxic tissues), systemic (IGF-1) or released by inflammatory reaction (IL1, TNF alpha and beta). One imagines usage of drugs which inhibit these factors and prevent angiogenesis. At the present time, two approaches have been used in proliferative retinopathy worsening despite panphotocoagulation; analogues of somatostatin and interferon alpha. The promissing results of these pilot studies have to be confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Outlook for the future in the treatment of diabetic retinopathy]. 752 51

Evidence for the presence of peptides, related to insulin-like growth factor 2 (IGF-2), has been obtained in the endocrine pancreas of the elasmobranchian species Raja clavata, the sting ray. By radioimmunoassay, IGF-2-like immunoreactivity was detected in Raja pancreas extract. Further characterization of this activity by acid gel chromatography revealed two distinct peaks of IGF-2-like immunoreactivity with apparent molecular weights of approximately 8.2 kDa and 4.5 kDa. Using the same IGF-2 antibody as well as antisera specific for mammalian IGF-1, insulin, glucagon, somatostatin and pancreatic polypeptide in double immunofluorescence studies, IGF-2-like immunoreactivity was located exclusively in insulin-immunoreactive cells. In contrast, IGF-1-like immunoreactivity was mainly observed in somatostatin- and glucagon-immunoreactive cells. A varying proportion (0-70%) of insulin-immunoreactive cells, however, displayed both IGF-1- and IGF-2-like immunoreactivity. Absorption studies indicated that the IGF-2-like peptides in Raja are different from mammalian and submammalian insulin and mammalian IGF-1, but similar to mammalian IGF-2. Thus, IGF-2-like peptides seem to occur during evolution as early as the phylogenetic development of the elasmobranchians. Furthermore, the results indicate a particularly conservative evolution of the islet IGF-2 system.
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PMID:IGF-2-like peptides are present in insulin cells of the elasmobranchian endocrine pancreas: an immunohistochemical and chromatographic study. 753 39

Twenty-three patients with active acromegaly underwent serum sampling for growth hormone (GH), insulin and insulin-like growth factor binding protein 1 (IGFBP-1) after placebo or single doses of octreotide or bromocriptine. Integrated 24-h serum GH levels decreased by 90% after octreotide and 49% after bromocriptine. A statistically significant correlation between the course of GH levels after octreotide and bromocriptine was observed (p < 0.001). Octreotide, but not bromocriptine, induced a significant increase in integrated 24-h serum IGFBP-1 levels to 37.4 times the baseline values. Bromocriptine caused a non-significant increase in integrated 24-h serum IGFBP-1 levels, which argues against a direct regulatory effect of GH on IGFBP-1 production in acromegaly. In conclusion, octreotide induces in acromegaly the production of IGFBP-1, which occurs independently of the number of somatostatin receptors on the GH-secreting pituitary adenoma. The supposed inhibitory effect of IGFBP-1 on the biological effect of IGF-1 might result in an additional clinical benefit in acromegalic patients as compared to treatment directed at the pituitary level.
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PMID:Octreotide, but not bromocriptine, increases circulating insulin-like growth factor binding protein 1 levels in acromegaly. 754 70

Acromegaly is a rare endocrine disorder characterized by growth hormone hypersecretion and is usually caused by a pituitary macroadenoma. It is associated with significantly increased patient morbidity and mortality. Molecular biological studies have implicated a causative role for oncogenic mutations (activating Gs alpha mutations and/or chromosomal 11q13 deletions) in less than 50% of cases. The cause(s) in the remaining 50% is speculative. Epidemiological evidence indicates that biochemical cure is achieved when mean GH levels are 5mU/l or less during a day-profile. This GH value correlates well with that required to normalize the serum IGF-1 concentration, a GH-dependent peptide which can be used to monitor the disease activity in acromegaly. Treatment must be carried out under the supervision of a dedicated endocrinologist and tailored to patients needs. The success of any treatment modality (surgery/pituitary irradiation/medical) depends on adenoma size and the extent of pretreatment GH hypersecretion. A combination of therapies is usually required to achieve satisfactory control of adenoma growth and GH hypersecretion. Octreotide, a synthetic analogue of native somatostatin, is particularly effective in controlling GH hypersecretion in this condition and the widespread introduction of a long-acting depot preparation is eagerly awaited. The development of true GH deficiency as a result of treatment is potentially worrying in view of its possible contribution to the increased incidence of cardiovascular mortality associated with hypopituitarism.
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PMID:Acromegaly: unravelling a complex disease. 758 Aug 62

Although receptors for somatostatin are found in bone cells, the effect of somatostatin analogs on calcium metabolism is unknown. The authors studied, in a metabolic ward, the effect of octreotide (a long-acting somatostatin analog) and a placebo in two 6-day calcium balance periods in 8 children with Duchenne muscular dystrophy. As expected, octreotide (2 micrograms/kg, subcutaneously, every 8 hours) reduced serum growth hormone and somatomedin (IGF-1) to levels found in growth hormone deficiency. Octreotide enhanced calcium retention by 30% (96 mg daily [P < 0.04]) in 7 boys for whom complete data (diet, urine, and fecal calcium) were available. In 6 children with urinary calcium excretion (Uca) greater than 50 mg daily, octreotide markedly lowered Uca, from 114 +/- 23 mg daily to 61 +/- 9 mg daily (P < 0.03). Calcium retention occurred in patients with or without initial hypercalciuria, but the higher the basal Uca, the greater was the inhibition by octreotide (r = 0.79; P < 0.03). Inactive, nonambulatory patients had a more pronounced response of Uca to octreotide (P < 0.02). Octreotide caused a mild, nonsignificant reduction in fecal calcium, with no major changes in serum calcium, phosphorus, parathyroid hormone, urinary excretion of sodium and potassium, or in creatinine clearance. Based on the current observations and the presence of receptors for somatostatin in bone cells, this hormone may have, at least on a short-term basis, an anabolic effect on calcium, perhaps favoring its deposition in bone.
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PMID:Octreotide enhances positive calcium balance in Duchenne muscular dystrophy. 766 11


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