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)

Eighteen patients with post-operative enterocutaneous fistulas were treated with total parenteral nutrition (TPN), skin care, infection control and intravenous somatostatin (SMS) 250 micrograms/h. This group was compared with 30 patients treated with standard medical treatment (total parenteral nutrition (TPN), skin care and infection control). In the SMS group the fistula output was reduced to 50% in three days and spontaneous closure was observed in 14 patients after a mean of 6.1 +/- 3.1 days of treatment with SMS, and in 18.2 +/- 6.3 days after the TPN administration. In the control group the fistula output was reduced by up to 50% after a week and spontaneous closure occurred in 20 patients in a mean of 27.4 +/- 8.7 days after the start of treatment. These results are statistically significant. There was one (5.5%) death in the SMS group compared with three (10%) deaths in the other, and glucose intolerance was observed in two (11%) patients in the SMS group. Somatostatin has been shown to be useful in the conservative treatment of enterocutaneous fistulas because of its ability to reduce output and accelerate closure.
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PMID:Treatment of enterocutaneous fistulas with TPN and somatostatin, compared with patients who received TPN only. 198 31

The effect of rioprostil, a methylprostaglandin E1 analog on circulating pancreatic hormones was evaluated in 13 healthy male subjects. Rioprostil administration, 300 micrograms twice daily resulted in a significant decrease of fasting insulin, C-peptide, glucagon, and pancreatic polypeptide. No change in fasting plasma glucose or somatostatin levels was observed. An oral glucose tolerance test induced similar increments in plasma glucose concentration before and during treatment, but a delayed rise of insulin and C-peptide levels occurred during the administration of the drug. On rioprostil, the glucose load no longer inhibited peripheral glucagon or somatostatin. Treatment with rioprostil remained without effect on mixed meal-induced changes in plasma glucose levels and concomitant increases in insulin, pancreatic polypeptide, and somatostatin levels. It is concluded that in healthy individuals rioprostil influences the basal and glucose-induced levels of glucagon, insulin, and somatostatin. In healthy men this effect did not, however, result in glucose intolerance.
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PMID:Effect of rioprostil, a methylprostaglandin E1 analog, on basal and stimulated plasma pancreatic hormone levels in man. 210 96

To examine glucose-stimulated insulin secretion and insulin sensitivity in the normal subjects and patients with impaired glucose tolerance, we performed the oral glucose tolerance test (OGTT) and modified insulin suppression test in 34 non-obese subjects. The plasma glucose and insulin concentrations were measured during fasting and every 30 min up to 120 min following 75 g of oral glucose loading. Ten subjects were classified as impaired glucose tolerance (IGT), and 24 subjects were as having normal glucose tolerance. In addition, the insulin-stimulated glucose uptake was estimated in all subjects by measuring the final 30 min steady-state plasma glucose (SSPG) of a continuous infusion of somatostatin, insulin and glucose for 4 hours (modified insulin suppression test). The mean plasma glucose concentrations of fasting and 60, 90, 120 min during OGTT study were significantly higher in the IGT subjects than in the normals. In addition, the mean incremental glucose areas under the curve during OGTT study were also greater in the IGT subjects than in the normals. The mean serum insulin concentrations were significantly higher at 90 and 120 minutes in the IGT patients than in the normals. During the modified insulin suppression test, the mean SSPG concentrations were significantly higher in the IGT patients than in the normals under the similar steady-state plasma insulin in both groups. There was a good correlation between the incremental insulin areas under the curve (OGTT) and the SSPG in the normal subjects (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of insulin secretion and insulin sensitivity between normal and impaired glucose tolerance subjects with normal fasting plasma glucose. 217 67

Ten patients (seven women, three men) with active acromegaly, five previously treated and five newly diagnosed, were included in an open-label prospective trial of 3 daily subcutaneous injections of the long-acting somatostatin analogue SMS 201-995 (Sandostatin) at increasing doses in order to obtain maximum growth hormone (GH) suppression. Four patients had received surgery, radiotherapy or bromocriptine. SMS 201-995 doses were increased in a stepwise fashion from 100 micrograms every 8 h (three times daily) to 200, 300 and finally 500 micrograms three times daily at monthly intervals if mean serum GH values failed to decrease to undetectable levels in over 75% of the samples. The optimal dose was maintained for up to 28 months. Significant clinical improvement of headache, soft tissue swelling, facial features, hyperhidrosis and paraesthesia occurred in all patients. Mean 12-h GH levels were significantly suppressed in four patients and fell to normal values in four. Suppression of GH levels was not achieved in two patients. Comparison of the mean interindividual GH values shows that the optimal efficacious dose is 100 micrograms t.i.d. in 7/10 patients. Somatomedin-C (SM-C) was also significantly reduced to below 50% of pretreatment levels in nine patients in whom it was measured. The subsequent increments of SMS 201-995 up to 500 micrograms three times daily did not produce further clinically relevant GH or SM-C suppression. Pituitary tumour shrinkage occurred in five patients. Thyroid function remained normal. Impaired glucose tolerance occurred in four patients. Side-effects (diarrhoea, abdominal discomfort) were mild and transient. Asymptomatic gallstones occurred in three patients on 1500 micrograms/day and one patient on 600 micrograms/day after 6-12 months treatment. This dose-finding study shows that 100 micrograms three times daily SMS 201-995 is an effective therapy for most of the acromegalic patients we treated.
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PMID:Clinical and biochemical effects of incremental doses of the long-acting somatostatin analogue SMS 201-995 in ten acromegalic patients. 220 Jun 20

Octreotide, an analog of somatostatin, is a valid tool for the cure of acromegalic disease. This compound has a prolonged half-life and is more selective than native somatostatin in suppressing growth hormone (GH) secretion. Octreotide, 100 micrograms tid sc, decreases GH levels and improves clinical symptoms in about 85% of acromegalic patients, lowering GH to below 5 ng/ml in 45% and to below 2 ng/ml in 17-21%. Octreotide normalizes somatomedin-C (IGF-I) levels in 36-50% of patients. The increase of dosage up to 1500 micrograms/day does not appear useful in poor responsive patients. No adverse effects on other endocrine functions submitted to hypothalamus-pituitary control have been observed. A slight shrinkage of the pituitary tumor is observed in 30-50% of cases. Octreotide therapy is well tolerated and side effects are usually mild. However the possibility of colelithiasis, liver damage and diabetes mellitus in patients with glucose intolerance must be taken into account. In conclusion octreotide is a useful complement to therapeutic means now used for the treatment of acromegaly.
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PMID:[Treatment of acromegaly with octreotide, a synthetic analog of somatostatin with extended action]. 227 11

A somatostatin analog (SMS 201-995) was used to treat symptomatic patients with a residual tumor burden of gastrinoma or medullary thyroid carcinoma and pathologic elevations of circulating marker peptides associated with these neuroendocrine tumors. Possible inhibitory effects of the analog on marker peptides, patients' symptoms, or tumor progression were studied in a dose-response protocol and during several months of self-injection of SMS 201-995. Both patients reported remarkable relief of secretory diarrhea and other symptoms, and serum gastrin was successfully suppressed by increasing doses of the analog. However, no effect was seen in reduction of hypercalcitoninemia. Morphologic imaging of residual tumor showed no progression of medullary thyroid carcinoma during treatment and, in the case of hepatic gastrinoma metastases, remarkable tumor regression was confirmed. No toxicity or glucose intolerance was experienced. Somatostatin analog shows promise for palliative management of endocrinologic symptoms due to neuroendocrine tumors, and an inhibitory effect can be measured in some but not all peptide markers. Further evidence of its negative trophic effect on tumor blood flow may suggest an antineoplastic potential, as well as palliative use of this new treatment.
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PMID:Somatostatin analog: effects on hypergastrinemia and hypercalcitoninemia. 243 92

Twenty-seven patients with postoperative enterocutaneous fistulas were treated with parenteral nutrition and SMS 201-995 (100 micrograms/8 hours, subcutaneously), a long half-life somatostatin analogue. At the time SMS 201-995 was started, 11 patients had low output fistulas (less than 1000 ml/48 hours), 11 patients had high output fistulas (above 1000 ml/48 hours), and 5 patients had fistulas sitting in large abdominal wall defects. Within 24 hours of treatment, a mean reduction of 55% of the fistula output was observed. Fistula site or output before treatment had no influence on the magnitude of output reduction. Spontaneous closure was achieved in 77% of the patients after a mean of 5.8 +/- 2.7 days of treatment with this drug. Two patients died (7.4%). Pain at the injection site was referred by 15% of the patients but no other side effects were observed. Glucose intolerance was not observed. SMS 201-995 has been shown to be very useful in the conservative treatment of enterocutaneous fistulas because of its ability to rapidly reduce fistula output and accelerate spontaneous closure.
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PMID:Treatment of 27 postoperative enterocutaneous fistulas with the long half-life somatostatin analogue SMS 201-995. 250 Sep

Peripheral levels of basal and tolbutamide-induced somatostatin have been measured in patients with diabetes or impaired glucose tolerance (IGT) and compared with those in normal individuals. Basal somatostatin was significantly higher in patients with Type 1 diabetes than in age-matched control subjects. This increase was most pronounced at diagnosis, and appeared to be related to metabolic control in insulin-treated patients. No increase was noted in patients with Type 2 diabetes or with IGT. Intravenous bolus injection of tolbutamide enhanced peripheral somatostatin levels in healthy volunteers in a biphasic manner. Patients with IGT also exhibited a biphasic response but the amplitude of the first phase was higher. No secretory response was detected in 27/29 Type 1 diabetic patients at diagnosis; a somatostatin response to tolbutamide became detectable again in Type 1 patients with normalization of their basal somatostatin levels but was then paradoxically related to poor blood glucose control. In Type 2 diabetes, basal somatostatin levels were similar to age-matched control subjects, but decreased upon intravenous tolbutamide administration.
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PMID:Basal and tolbutamide-induced plasma somatostatin in healthy subjects and in patients with diabetes and impaired glucose tolerance. 256 79

The effect of hyperglycemia on glucose kinetics was investigated in normal and T4-treated miniature pigs. 1. T4-treatment increased basal plasma glucose (G) (+ 20%) and glucose turnover (+36%). 2. Glucose infusion (2 mg/kg x min) in controls increased insulin and glucose utilization (Rd), but decreased glucagon and hepatic glucose production (Ra). After T4-treatment glucose increased insulin, decreased glucagon and Ra but only a slight effect on G and Rd were observed. 3. Infusing glucose + somatostatin resulted in hyperglycemia in both groups due to an initial fall in Ra and Rd followed by an increase in Rd, where total Ra (endogenous + exogenous exceeded Rd. Glucose intolerance was more pronounced in controls, due to a T4-induced increase in Rd. During this non-steady state the increment in Rd per increment in G was calculated and showed 1.5 in controls and 2.5 after T4-treatment. These data give evidence that thyroid hormones increase glucose utilization during hypoinsulinemia.
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PMID:Glucoregulatory function of thyroid hormones: evidence for an insulin-independent effect. 257 Jul 10

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.
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PMID:Pancreatic islet hormone response to oral glucose in morbidly obese patients. 286 Aug 76


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