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)

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Angiopeptin, a somatostatin analogue, inhibits intimal hyperplasia after percutaneous transluminal coronary artery balloon angioplasty (PTCA) in several animal models. This pilot study sought to determine the effect of subcutaneous infusion of angiopeptin on clinical events and restenosis in patients undergoing successful PTCA. One hundred twelve patients were randomized to receive continuous subcutaneous angiopeptin (750 micrograms/day) or placebo infusion from the day before PTCA and for the following 4 days in a double-blind study. An additional subcutaneous injection of 375 micrograms of angiopeptin or saline was given immediately before PTCA. Eighty patients had a successful PTCA, and 75 of these patients with 94 lesions underwent angiography 6 +/- 2 months after PTCA. All 112 patients underwent a 12-month clinical follow-up examination. Age, sex, smoking, diabetes, hypertension, hyperlipidemia, and morphologic features of stenosis were similar in both groups. The hierarchical 12-month event rate (death, myocardial infarction, coronary artery bypass grafting, and repeated PTCA) was reduced from 34% to 25% (p = 0.30) by angiopeptin by intention-to-treat analysis. Restenosis (> or = 50% diameter stenosis) was significantly reduced in lesions treated with angiopeptin (12% vs 40%; p = 0.003). Late lumen loss also was significantly reduced after angiopeptin treatment (0.12 +/- 0.46 mm vs 0.52 +/- 0.64 mm; p = 0.003). In conclusion, continuous subcutaneous angiopeptin infusion for 5 days tended to decrease clinical events and restenosis after PTCA.
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PMID:Randomized double-blind Scandinavian trial of angiopeptin versus placebo for the prevention of clinical events and restenosis after coronary balloon angioplasty. 761 Oct 96

Angiopeptin is a long-acting cyclic octapeptide with pharmacologic actions clearly resembling those of the natural hormone somatostatin, but with different binding affinities for the five known somatostatin receptors. It is a potent inhibitor of myointimal migration and proliferation in animal models of angioplasty and organ transplantation. Experimentally, angiopeptin inhibits transplant arteriosclerosis in cardiac, renal and vascular allografts. The mechanisms are thought to involve abrogation of the increase of insulin-like growth factor (IGF-I) and other growth factors that occur in the vascular wall following immune or mechanical injury. Angiopeptin also restores the endothelium-dependent vasodilatory response to acetylcholine. Clinically, angiopeptin is safe in cardiac transplant patients and shows promise in inhibiting coronary transplant arteriosclerosis. Furthermore, in large clinical trials, angiopeptin (given as a continuous infusion for 5 days) inhibits serious clinical events, such as myocardial infarction, death and revascularization at 6 and 12 months following percutaneous transluminal coronary angioplasty. It has few serious side effects.
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PMID:Angiopeptin: experimental and clinical studies of inhibition of myointimal proliferation. 858 76

Angiopeptin, a somatostatin analogue, inhibits intimal hyperplasia after (percutaneous transluminal coronary angioplasty) (PTCA) in several animal models. This pilot study sought to determine the effect of subcutaneous infusion of angiopeptin on clinical events and restenosis in patients undergoing successful PTCA. One hundred and twelve patients were randomized to receive continuous subcutaneous angiopeptin (750 micrograms/day) or placebo infusion from the day before PTCA and for the following four days in a double-blind study. Eighty patients had a successful PTCA, and 75 of these patients with 94 lesions underwent angiography 6 +/- 2 months after PTCA. All 112 patients underwent clinical follow-up at 12 months. The 12-month event rate (death, myocardial infarction, coronary artery bypass grafting and re-PTCA) was reduced from 34% to 25% (p = 0.30) by angiopeptin by intention to treat analysis. Restenosis (> or = 50% diameter stenosis) was significantly reduced in lesions treated with angiopeptin (12% vs 40%; p = 0.003). Late lumen loss was also significantly reduced after angiopeptin treatment (0.12 +/- 0.46 mm vs 0.52 +/- 0.64 mm; p = 0.003). In conclusion, continuous subcutaneous angiopeptin infusion for five days tended to decrease clinical events and restenosis after PTCA.
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PMID:[Angiopeptin versus placebo for reductin of restenosis after PTCA treatment. A randomized, double-blind study]. 896 26

The international workshop on metaiodobenzylguanidine (MIBG) and radiolabeled somatostatin analogs held in Rome in June, 1994 addressed a wide range of topics which might be classified into five broad general themes: Theme 1. The role of MIBG for the location of neuroendocrine tumors. A) The range of tumors in which MIBG scintigraphy is effective (pheochromocytomas, neuroblastoma, chemodectoma and other APUDomas). B) The increasing popularity of 123I as a radiolabel for MIBG (potential advantages in planar and SPECT imaging). C) MIBG as the prototype of a family of radiopharmaceuticals exploiting the biogenic amine uptake and storage mechanisms. (Other radiohalides 124I, 125I, 87Br, 211At, 18F; other PET radiopharmaceuticals such as 11C-epinephrine, 11C-hydroxyephedrine). Theme 2. The role of MIBG as an in vivo scintigraphic probe of the sympathetic nervous system. A) Cardiac sympathetic innervation (in cardiomyopathy, myocardial infarction, and as a prognostic index for cardiac transplantation). B) Pulmonary MIBG uptake as index of pulmonary endothelial/sympathetic function (MIBG by both the intravenous and inhaled routes of administration). Theme 3. MIBG for the radiopharmaceutical therapy of neuroendocrine tumors. A) Treatment of neuroblastoma early in the natural history of the disease (MIBG therapy as initial management, MIBG therapy combined with other modalities--e.g., chemotherapy and bone marrow transplantation). Theme 4. The role of radiolabeled somatostatin analogs for the location of neuroendocrine and other tumors. A) The range of tumors in which somatostatin receptor radiopharmaceutical scintigraphy is effective (pituitary tumors, central nervous system tumors, carcinoids, islet cell tumors, medullary thyroid carcinoma, small cell lung cancer, APUDomas). B) The superiority of 111In over 123I as a radiolabel (the future of potential 99mTc and other labels). C) Somatostatin receptor scintigraphy in autoimmune and other disorders. D) Pentetreotide as the prototype of a wide range of radiolabeled peptides as radiopharmaceuticals for the in vivo depiction of the receptors for peptide hormones, lymphokines, paracrine and other information transmitting molecules (the general concepts include the use of long-acting, slowly degraded analogs and the development of generally applicable labeling techniques. Examples include 123I-ANF, labeled interleukins and other lymphokines). Theme 5. Comparisons of MIBG and pentetreotide scintigraphy for the location of neuroendocrine tumors. A) The range of neuroendocrine and other tumors (e.g., pheochromocytomas, neuroblastomas, carcinoids, islet cell tumors and other APUDomas).
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PMID:Ten years of experience with MIBG applications and the potential of new radiolabeled peptides: a personal overview and concluding remarks. 900 76

Urotensin II (UII) is a somatostatin-like peptide recently identified as a potent vasoconstrictor. In this study, we examined whether UII promotes cardiac remodeling through nonhemodynamic effects on the myocardium. In a rat model of heart failure after myocardial infarction (MI), increased UII peptide and UII receptor protein expression was observed in both infarct and noninfarct regions of the left ventricle compared with sham. Moreover, post-MI remodeling was associated with a significant 75% increase in UII receptor gene expression in the heart (P<0.05 versus sham controls), with this increase noted in both regions of the left ventricle. In vitro, UII (10-7 mol/L) stimulation of neonatal cardiac fibroblasts increased the level of mRNA transcripts for procollagens alpha1(I), alpha1(III), and fibronectin by 139+/-15% (P<0.01), 59+/-5% (P<0.05), and 141+/-14% (P<0.01), respectively, with a concomitant 23+/-2% increase in collagen peptide synthesis as determined by 3H-proline incorporation (P<0.01). UII had no effect on cellular hypertrophy, as determined by changes in total protein content in isolated neonatal cardiomyocytes. However, expression of recombinant rat UII receptor in neonatal cardiomyocytes resulted in significant UII-dependent activation of hypertrophic signaling as demonstrated by increased total protein content (unstimulated, 122.4+/-4.0 microg/well; rat UII, 147.6+/-7.0 microg/well; P<0.01) and activation of the hypertrophic phenotype through Galpha(q)- and Ras-dependent pathways. These results indicate that, in addition to potent hemodynamic effects, UII may be implicated in myocardial fibrogenesis through increased collagen synthesis by cardiac fibroblasts and may also be an important determinant of pathological cardiac hypertrophy in conditions characterized by UII receptor upregulation.
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PMID:Direct actions of urotensin II on the heart: implications for cardiac fibrosis and hypertrophy. 1284 17

Active acromegaly is associated with significant comorbidity and reduced quality of life. However, the prevalence of comorbidity after long-term remission is not established. Therefore, we assessed the presence of comorbidity in 118 patients in long-term remission after surgery, radiotherapy, and/or somatostatin analog treatment according to strict biochemical criteria of serum GH and IGF-I concentrations and evaluated the impact of comorbidity on quality of life. The mean duration of remission was 12.0 +/- 7.4 yr, and mean actual IGF-I sd scores were 0.6 +/- 1.7. Self-reported joint problems occurred in 77% of patients, hypertension in 37%, a history of myocardial infarction in 9%, and diabetes mellitus in 11%. The presence of joint problems was not related to GH and IGF-I levels, active disease duration, or age. Joint complaints had significant negative impact on quality of life. Patients with a history of myocardial infarction had reduced scores for general health, depression, and fatigue, and diabetes mellitus was associated with reduced scores for anxiety and sleep. In conclusion, acromegalic patients had a high prevalence of joint-related comorbidity and hypertension despite long-term control of GH excess. Especially, joint complaints contributed to a reduced perceived quality of life in these patients.
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PMID:Morbidity after long-term remission for acromegaly: persisting joint-related complaints cause reduced quality of life. 1574 Dec 57

We tested the hypothesis that octreotide, a somatostatin analogue, can mimic ischemic preconditioning (PC) to provide cardioprotection against myocardial infarction. An ischemia-reperfusion model of adult Wistar rats was used. Infarct size was expressed as a percentage of the area at risk under different treatment protocols. Octreotide PC (35 microg/Kg 20 minutes before ischemia-reperfusion) significantly decreased infarct size (18 +/- 4%) versus control (60 +/- 7%). The somatostatin receptor antagonist cyclo-somatostatin (0.5 mg/Kg) could blunt the above cardioprotection. Administration of either chelerythrine (a protein kinase C inhibitor, 2 mg/Kg) or genistein (a tyrosine kinase inhibitor, 5 mg/Kg) could also block octreotide PC (54 +/- 7% and 58 +/- 6%, respectively). Pretreatment with the mitochondrial ATP-sensitive potassium channel antagonist 5-hydroxydecanoic acid (5-HD) and the sarcolemmal ATP-sensitive potassium channel antagonist glibenclamide could abolish the effects of octreotide PC (54 +/- 6% and 52 +/- 6%). Chelerythrine, however, had no effect on octreotide PC. In conclusion, the present study demonstrates that octreotide can mimic ischemic PC to reduce infarct size. Acute effects of octreotide PC involve the activation of protein kinase C, tyrosine kinase C, and mitochondrial ATP-sensitive potassium channels, but not systemic IGF-I activation.
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PMID:Somatostatin analogue mimics acute ischemic preconditioning in a rat model of myocardial infarction. 1577 21

Extrapituitary roles for hypothalamic neurohormones have recently become apparent and clinically relevant, based on the use of synthetic peptide analogs for the treatment of multiple conditions including cancers, pulmonary edema and myocardial infarction. In the eye, it has been suggested that some of these hormones and their receptors may be present in the ciliary body, iris, trabecular meshwork and retina, but their physiological role has yet to be elucidated. Our study intends to comprehensively demonstrate the expression of some hypothalamic neuroendocrine hormones and their receptors within different retinal and extraretinal structures of the human eye. Immunofluorescence, Western blot analysis, and RT-PCR were used to evaluate the qualitative and quantitative expression of Luteinizing Hormone Releasing Hormone (LHRH), Growth Hormone Releasing Hormone (GHRH), Thyrotropin Releasing Hormone (TRH), Gastrin Releasing Peptide (GRP) and Somatostatin as well as their respective receptors (LHRH-R, GHRH-R, TRH-R, GRP-R, SST-R1) in cadaveric human eye tissue and in paraffinized human eye tissue sections. The hypothalamic hormones LHRH, GHRH, TRH, GRP and Somatostatin and their respective receptors (LHRH-R, GHRH-R, TRH-R, GRPR/BB2 and SST-R1), were expressed in the conjunctiva, cornea, trabecular meshwork, ciliary body, lens, retina, and optic nerve.
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PMID:Expression of hypothalamic neurohormones and their receptors in the human eye. 2897 97