Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine patients with psoriasis vulgaris were treated for 12 weeks with somatostatin analog, octreotide acetate (SMS 201-995) 50 or 100 micrograms by subcutaneous injection every 12 hours. The purposes of the study were to determine: (1) levels of insulin, glucose, glucagon, pancreatic polypeptide (PP), and SMS 201-995 after a subcutaneous injection of SMS 201-995 and ingestion of a standardized meal; (2) nocturnal (0200 h) thyroid stimulating hormone (TSH) levels before, during, and after treatment; and (3) the pharmacokinetics of SMS 201-995. Insulin peaks at 30 minutes were blunted from 65.8 +/- 11.0 mu U/mL without treatment to 26.7 +/- 8.6 mu U/mL and 7.7 +/- 2.0 mu U/mL after the 50- and 100-micrograms doses, respectively. Glucagon levels remained constant during the meal and were not affected by the 50-micrograms dose. Mean glucose levels were significantly elevated during insulin suppression. PP was also rapidly suppressed by SMS 201-995 and remained so for 4 hours after the injection. Nocturnal TSH was blunted after 12 weeks of treatment (P less than or equal to .05). T4 and T3 resin uptake showed no depression, and patients remained clinically euthyroid. The plasma peak of SMS 210-995 occurred 30 minutes postinjection and half-life was longer than 2 hours. After chronic administration of SMS 201-995, insulin was suppressed with resultant mild carbohydrate intolerance that persisted throughout the treatment course.
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PMID:Treatment of psoriasis with chronic subcutaneous administration of somatostatin analog 201-995 (sandostatin). II. Effect on pancreatic and thyroid hormone. 240 89

The effect of a long-acting somatostatin analogue on the acute renal hypertrophy following induction of experimental diabetes in the rat has been studied. The kidney weight increase occurring at 2 and 7 days after alloxan injection was significantly lower in the diabetic group receiving somatostatin. Similarly, the previously reported increase in glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and 6-phosphogluconate dehydrogenase (EC 1.1.1.44) found in the kidney at 2 and 7 days of diabetes was less marked in the group receiving SMS 201-995. The fall in renal phosphoribosyl pyrophosphate associated with early diabetic renal hypertrophy (7) was also lessened by administration of SMS 201-995. No effects of the drug were found in the normal rat on the same regimen of treatment. These observations indicate involvement of glucagon and/or growth hormone in the initiation of kidney growth in diabetes.
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PMID:The effect of a somatostatin analogue (SMS 201-995, Sandostatin) on the concentration of phosphoribosyl pyrophosphate and the activity of the pentose phosphate pathway in the early renal hypertrophy of experimental diabetes in the rat. 245 25

The effect of SMS 201-995, a long-acting somatostatin analogue, on splanchnic blood flow and glucose metabolism, was investigated in five groups of healthy subjects. Groups A (n = 4), B (n = 5), C (n = 5) and D (n = 5) were studied before, during and after a 60-min intravenous infusion of SMS (1.7, 0.8, 0.2 and 0.1 micrograms min-1, respectively). Group E (n = 6) was investigated before and for 6 h after a subcutaneous injection of 25 micrograms of SMS. The splanchnic blood flow decreased by 20-25% in all groups in response to SMS and remained low during the entire observation periods. Arterial concentrations of glucose showed a 15-20% decline during SMS infusion in Groups A and B (P less than 0.05-0.01) and a less pronounced decrease in the other groups. Fifteen minutes after the end of infusion the glucose levels started to rise and in group A, the levels were significantly higher than basal (+25%, P less than 0.05-0.01) at 90-180 min after the end of infusion. The net splanchnic glucose production, determined in groups A and B, decreased by 65-75% in response to SMS infusion. Towards the end and immediately after the infusions, however, the net glucose output increased, but decreased again at 30-60 min after the end of infusion. Arterial, insulin and glucagon concentrations decreased significantly during infusion in all groups. This decline was more pronounced for insulin (50%) than for glucagon (20-25%) and insulin concentrations remained low for a longer period after the end of infusions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous and subcutaneous administration of a long-acting somatostatin analogue: effects on glucose metabolism and splanchnic haemodynamics in healthy subjects. 249 81

We report 1 patient with a necrolytic migratory erythema, a high plasma glucagon concentration and a metastatic pancreatic endocrine tumor who has now been treated effectively for 33 months with the somatostatin analogue octreotide (SMS 201-995) (400 micrograms/day). The results of SMS 201-995 in the treatment of glucagonoma syndrome are reviewed.
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PMID:Octreotide (SMS 201-995) in the treatment of metastatic glucagonoma: report of one case and review of the literature. 254 11

SMS 201-995 (Sandoz Pharmaceuticals, East Hanover, NJ) is a synthetic peptide analog of native somatostatin that has been used to relieve symptoms caused by neuroendocrine tumors. Reports have described an insulin suppressive effect of SMS 201-995 that results in elevations of blood glucose. We report a patient with a metastatic small bowel carcinoid and renal failure in whom mild symptomatic hypoglycemia occurred 30 to 60 minutes after SMS 201-995 administration. No increase in insulin or decreases in glucagon, cortisol, or catecholamines were observed during these hypoglycemic episodes. Elevated levels of growth hormone fell gradually following SMS 201-995 administration and did not temporally correspond to the 30- to 60-minute nadir of blood glucose. However, SMS 201-995 levels peaked during this 30- to 60-minute period. As clinical experience with this drug broadens, patients whose glucose control is dependent on counter-regulatory hormones should be monitored for the possibility of hypoglycemia.
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PMID:Hypoglycemia after administration of somatostatin analog (SMS 201-995) in metastatic carcinoid. 260 30

GH has been implicated in the pathophysiology of various acute and chronic complications of diabetes mellitus. As a consequence, there has been a great deal of interest in developing methods for suppressing GH secretion in diabetes. SMS 201-995 is a long-acting somatostatin analog which inhibits the secretion of numerous hormones, including GH. To determine the metabolic and hormonal responses to SMS 201-995 independent of endogenous insulin suppression, we studied six patients with insulin-dependent diabetes mellitus while they received 150 micrograms SMS 201-995, sc, daily for an 8-week period. This treatment resulted in no change in 24-h glucose profiles, although the mean insulin dose decreased by 19%, while hemoglobin A1c decreased significantly (0.084 +/- 0.023 to 0.067 +/- 0.011, P = 0.04). The 24-h profiles of blood lactate, plasma free insulin, glucagon, FFA, blood glycerol, and beta-hydroxybutyrate were unchanged, whereas that of blood alanine increased significantly (7.8 +/- 0.4 to 10.6 +/- 0.9 mmol/L.h; P = 0.01). GH secretion declined in five of the six patients; the mean values before and during SMS 201-995 treatment were 102 +/- 23 and 68 +/- 12 micrograms/L.h, respectively (P = NS), for the six patients. [In the five patients in whom GH secretion declined, the mean values before and during SMS 201-995 treatment were 115 +/- 23 and 63 +/- 14 micrograms/L.h, respectively (P = 0.01).] These results suggest that SMS 201-995 may be administered to patients with insulin-dependent diabetes mellitus without a deleterious effect on metabolic control.
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PMID:The effects of SMS 201-995 (sandostatin) on metabolic profiles in insulin-dependent diabetes mellitus. 264 88

We evaluated the effectiveness of a more potent and longer-acting somatostatin analogue (SMS 201-995) as an adjunct to insulin therapy, in a double-blind placebo-controlled randomized study of 26 C-peptide-negative type I (insulin-dependent) diabetic patients (20 women, 6 men, aged 22-40 yr) on their conventional drug regimens for 12 wk. Eight patients received a low dose (10 micrograms) of the analogue, 9 received a high dose (50 micrograms) of the analogue, and 9 received placebo subcutaneously before breakfast and dinner. Twenty-four-hour serum glucose, free insulin, plasma growth hormone (GH), and glucagon profiles were obtained before and during treatment at 4-wk intervals. The mean age, duration of diabetes, daily insulin dose, and body weight were not significantly different among the groups. The mean weekly capillary blood glucose values and exogenous insulin requirements were not changed by the SMS 201-995 therapy. Mean glycosylated hemoglobin A1 levels were unchanged in both the analogue- and placebo-treated groups at wk 12. Basal and postprandial glucose, free insulin, GH, and glucagon profiles were not influenced by the SMS 201-995 therapy throughout the study. Nocturnal glucose turnover rates (D-[3-3H]glucose technique) remained unaltered by the analogue therapy. Dose-dependent gastrointestinal (GI) adverse effects (e.g., diarrhea) were documented in the analogue-treated patients. Visual acuity and fundic photomicrographs of our patients were not changed by the analogue therapy. In conclusion, the prominent adverse GI effects our patients experienced preclude the use of larger doses of the analogue that may be necessary to suppress GH and glucagon and improve glucose control in type I diabetic patients.
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PMID:Metabolic effects of long-acting somatostatin analogue (sandostatin) in type I diabetic patients on conventional therapy. 265 40

We studied the effects of a premeal sc injection of an analog of somatostatin (SMS 201-995, Sandoz) on the postprandial glycemic excursions, insulin requirement and hormone profiles (GH, glucagon and C-peptide) in 8 IDDM patients (diabetes duration 14.0 +/- 6.5 yr, daily insulin requirement 36 +/- 6.4 U) maintained normoglycemic by connecting them to a closed-loop insulin infusion system (Betalike, Genoa). The morning of the test the patients were connected to the Betalike and their glucose levels stabilized for at least 4 h. At 13:00 h the study was begun with a sc injection of 50 micrograms of SMS 201-995 or placebo (randomly) and a standardized mixed meal (800 Kcal) was given. Blood samples were obtained 0, 15, 30, 60, 120 and 180 min after the injection. Each patient was tested both with SMS 201-995 and placebo. Postmeal glycemic peaks were decreased after SMS 201-995 (119.6 +/- 5.4 mg/dl vs 149.1 +/- 4.2; p less than 0.05) as well as insulin requirements (3.2 +/- 0.8 U vs 13.3 +/- 1.9; p less than 0.01) for the 180 min postprandial period. Similarly, glucagon level was reduced 30 min postprandially (24 +/- 6 pg/ml vs 59 +/- 24; p less than 0.05) and so GH level only 180 min after lunch (p less than 0.05). The premeal injection of SMS decreases postprandial glycemic excursions and the corresponding insulin requirement. The action of SMS 201-995 may be mainly mediated by the suppression of postprandial glucagon peak.
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PMID:Effects of a somatostatin derivative (SMS 201-995) on postprandial hyperglycemia in insulin-dependent diabetics studied by means of a closed-loop device. 267 Nov 12

With the aim of assessing a new somatostatin analogue to prevent the metabolic changes induced by a 6-h nocturnal arrest of an insulin pump, nine C-peptide negative Type 1 (insulin-dependent) diabetic patients were submitted blindly to two interruptions (from 23.00 to 05.00 hours) of their continuous s.c. insulin infusion, once after a single s.c. injection at 23.00 hours of 50 micrograms SMS 201-995 (Sandostatin, Sandoz) and once after 0.9% NaCl. Plasma SMS 201-995 levels peaked at 24.00 hours and then declined with an elimination half-life averaging 144 +/- 15 min. Plasma glucagon and growth hormone levels were significantly reduced after SMS 201-995 whereas the progressive fall in plasma-free insulin levels from 23.00 to 05.00 hours was unaffected. In the control test, blood glucose levels tended to decrease slightly from 23.00 to 02.00 hours and then increased markedly from 02.00 to 05.00 hours (+5.3 +/- 1.5 mmol/l) while after SMS 201-995 they decreased significantly from 23.00 to 02.00 hours (-2.6 +/- 0.5 mmol/l), resulting in values below 3 mmol/l in seven subjects, but showed a secondary increase until 05.00 hours (+3.5 +/- 1.5 mmol vs 23.00 h; p less than 0.05 vs 0.9% NaCl). While the rises in plasma non-esterified fatty acid and glycerol levels were not reduced by SMS 201-995, the increase in plasma 3-hydroxbutyrate levels, although similar from 23.00 to 02.00 hours, was significantly reduced from 02.00 to 05.00 hours (+77 +/- 20 vs +124 +/- 31 mumols.l-1.h-1; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sandostatin, a new analogue of somatostatin, reduces the metabolic changes induced by the nocturnal interruption of continuous subcutaneous insulin infusion in type 1 (insulin-dependent) diabetic patients. 268 64

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 micrograms subcutaneously), in seven patients with chronic autonomic failure. 2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged. 3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase. 4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.
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PMID:Prevention of glucose-induced hypotension by the somatostatin analogue octreotide (SMS 201-995) in chronic autonomic failure: haemodynamic and hormonal changes. 269 Nov 74


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