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)

6 normal subjects received two times of 2 hr euglycemic glucose clamp studies (insulin infusion rate 40 mU/M2/min) one with and the other without somatostatin (SRIF) infusion (500 microgram/hr). Serum C-peptide and glucagon levels were measured during clamp to study the sensitivity of pancreatic alpha and beta cells to the suppressive effects of exogenous hyperinsulinemia during normoglycemia in normal subjects and to find whether SRIF had any modulative effects on endocrine pancreas secretion at the status of hyperinsulinemia. The results showed that in normal man the degree of suppression of pancreatic glucagon secretion by hyperinsulinemia (approximately 100 uU/ml) during euglycemic glucose clamp without SRIF infusion was less than that of C-peptide with mean value of 62 +/- 4% of basal glucagon remained at the end of clamp study; while only about 30 +/- 2% of basal C-peptide concentrations remained. But during SRIF infused glucose clamp studies (SRIF was infused from 60 to 120 min), 32 +/- 2% of mean basal C-peptide concentrations and 38 +/- 6% of mean basal glucagon concentrations left at the end of 2 hr clamp studies when serum insulin level was about 100 uU/ml. For the glucose infusion rate (M value), it was significantly greater in our normal subjects in response to insulin + SRIF as compared to insulin alone (12.0 + 0.9 vs 8.8 +/- 1.4; P less than 0.01). We concluded: during hyperinsulinemia (100 uU/ml), the sensitivity of pancreatic alpha cells to insulin seems less than that of beta cells in normal man at normoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pancreatic glucagon and C-peptide secretion during hyperinsulinemia in euglycemic glucose clamp with or without somatostatin infusion in normal man. 288 1

The effect of jejunoileal bypass in lean and obese Zucker rats on a number of enteroendocrine cell types was investigated 5 weeks following surgery to remove 80 percent of the small bowel from continuity. The endocrine cells containing somatostatin, cholecystokinin, gastric inhibitory polypeptide, enteroglucagon and neurotensin were investigated. In control rats enteroglucagon cell number was decreased in obese compared to lean animals (5 +/- 1 vs 11 +/- 1 cells/mm). Following jejunoileal bypass the enteroglucagon cell population increased two-fold in both the functional and bypassed bowel in obese rats but was not elevated in lean animals. A significant increase in the number of cholecystokinin cells in the bypassed loop of the jejunum in both lean and obese bypassed rats was observed. The cholecystokinin cell population was also markedly elevated in the functional jejunum of obese but not lean bypassed rats. Only small changes were noted in cell numbers of gastric inhibitory polypeptide, somatostatin and neurotensin containing cells, suggesting that individual cell types have specific stimuli for proliferation. Epithelial height, a measure of intestinal adaptation, was similar in lean and obese rats in both the control and bypassed states, but weight loss in obese bypassed animals was significantly greater than that of lean bypassed rats. The hyperinsulinemia of obese rats was only partially normalized by jejunoileal bypass. These data indicate that jejunoileal bypass has effects on specific enteroendocrine cells which differ between lean and obese Zucker rats, and between individual cell types.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of jejunoileal bypass (JIB) in the obese Zucker rat on a sub-group of enteroendocrine cells. 288 90

Four infants (three boys and one girl, ages 12-89 days) with persistent hyperinsulinism secondary to nesidioblastosis (two) or microadenoma of the pancreas (two) were treated with cyclic somatostatin (S) as part of the preoperative management until subtotal pancreatectomy was performed within 12 to 35 days. The individual dose dependent response of glucoregulatory hormones to exogenous was evaluated by means of the "somatostatin sensitivity test" (SST). Thereby S was infused in stepwise increasing doses, as dictated by the prevailing blood glucose levels, until normoglycemia was achieved concomitantly with a dextrose infusion at rates of 5 mg/kg/min. This procedure resulted only in a partial suppression of insulin, C-peptide, glucagon, HGH and cortisol, without recurrence of hypoglycemia. Compared to baseline levels, plasma concentrations of insulin decreased by 61%, of C-peptide by 64% and a rise of glucagon by 23% was observed. The SST which can be performed under routine clinical conditions, is a useful procedure for evaluating the individual S-dose necessary to achieve normoglycemia. The risk of total S-induced suppression of hormones, such as IRI, IRCP, HGH, glucagon and cortisol can be omitted.
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PMID:[Preoperative management of newborn infants with hyperinsulinemic hypoglycemia (2)]. 289 Jul 92

The use of somatostatin in the treatment of a newborn infant with hyperinsulinism is reported. When administered alone, somatostatin was only able to prevent hypoglycemia for a short period of time, whereas the addition of a constant infusion of glucagon allowed successful control of the patient's hypoglycemia. As hyperinsulinism relapsed after a subtotal pancreatectomy, a trial was carried out with a somatostatin analog, which has an expected longer duration of action. It led to a significant rise in the blood glucose level but failed to prevent safely hypoglycemia even when 4 injections were performed daily.
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PMID:[Somatostatin in a case of neonatal hyperinsulinism caused by focal adenomatosis of the head of pancreas]. 289 21

Somatostatin participates in the regulation of nutrient entry from the intestinal tract into the circulation. Thus, dietary fats and proteins may elicit significant increases of gastropancreatic somatostatin. Regulation of postprandial somatostatin secretion may occur via neural, hormonal and humoral factors. This peptide, in pharmacological doses, inhibits virtually all gastrointestinal exo- and endocrine functions as well as local motor activity. Neutralization of endogenous circulating somatostatin with specific antiserum is followed by increases in GH and enteroglucagon, augmenting also the postprandial rise of gastrin, insulin and pancreatic polypeptide. Somatostatin deficiency can be observed in obese subjects with hyperinsulinism. Concomitant elevation of insulin and gastrin levels can be antagonized by exogenous somatostatin. These findings confirm the importance of somatostatin as a peripheral regulator in experimental and human biology.
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PMID:Physiological significance of gastrointestinal somatostatin. 290 Feb

In 59 patients suffering from chronic psoriasis, we tested the therapeutic effects of yohimbine and colchicine. It is well known that yohimbine, an alpha 2-adrenoceptor-blocking agent, reduces the secretion of insulin and the platelet factors. 85% of our psoriatic patients showed decreased values for somatostatin, in association with hyperinsulinemia (88%) and low platelet counts. Successful therapy with yohimbine resulted in the normalization of the pathological blood levels.
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PMID:[Somatostatin deficiency, hyperinsulinism and thrombocyte aggregation in psoriasis]. 290 97

Unlike its lethal exocrine counterpart, islet cell carcinoma of the pancreas is an indolent neuroendocrine neoplasm. The majority of these tumors are hormonally active. When functioning, a number of clinical syndromes (for example, hyperinsulinism, Zollinger-Ellison and Cushing's syndromes) may be evident. Fifty-eight patients surgically treated between 1965 and 1984 were retrospectively analyzed. The purpose of this study was to determine the distribution of functioning versus nonfunctioning tumors and the response to type of therapy. Mean postoperative follow-up was 7.4 years. Survival and prognostic indices were calculated by the Kaplan-Meier method and compared with log-rank tests. Of the group, 54% had functioning and 46% nonfunctioning tumors. Gastrinomas were the most common functioning tumors encountered (19%). Of interest was the finding that nonfunctioning tumors increased steadily during the last 15 years of the study (25% to 65%). Curative resections were performed in 15 (26%) and noncurative procedures in 43 patients (74%), with an overall operative mortality rate of 3%. Symptomatic improvement was achieved in 90% (curative) and 51% (noncurative). Survival at 3 years was 87% and 66% for the curative and noncurative groups, respectively (p less than 0.1), with an overall 5-year survival of 42%. The absence of hepatic metastases was a major predictor of survival at 3 years (82% vs 56%, p less than 0.05). Survival was statistically better at 3 years in those patients with gastrinomas compared with patients with nonfunctioning tumors (91% vs 58%, p less than 0.05). Although surgical cure is rare, significant long-term palliation may be achieved in a large percentage of patients with an aggressive surgical approach, occasional total gastrectomy, combination chemotherapy, H2 blockade, when indicated, and, most recently, with the new long-acting analogue of somatostatin.
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PMID:Islet cell carcinomas of the pancreas: a twenty-year experience. 290 80

The aim of the present study was to evaluate various functional tests for the differentiation of hyperinsulinaemic hypoglycaemia. The pathophysiological and histological findings in six infants, aged 2-7 months, with persistent hyperinsulinaemic hypoglycaemia are described. Islet cell adenoma was found in four infants and pancreatic nesidioblastosis in two others. Circulating levels of blood glucose (BG), immunoreactive insulin and C-peptide immunoreactivity were measured under basal conditions and during both stimulation and suppression. The diagnosis of hyperinsulinaemia was made by estimation of the BG/serum insulin ratio, which was the most important diagnostic criterion of hyperinsulinism. Control subjects of comparable age showed a ratio of 8.3 +/- 4.4 (range 4.1-13.3), whereas the six patients had values between 0.3 and 5.1. At least four determinations with ratios lower than 2.6 were necessary for confirming the diagnosis. Preoperatively we performed oral glucose tolerance, diazoxide infusion, somatostatin infusion and C-peptide suppression tests. It is suggested that the various function tests, especially the suppression tests, do not differentiate hyperinsulinism caused by an adenoma from that caused by diffuse pancreatic nesidioblastosis.
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PMID:The hyperinsulinaemic hypoglycaemias in infancy: a study of six cases. 290 71

Hypothalamic somatostatin concentration was determined in 6.5 to 9 months old male and female genetically obese fatty (fa/fa) and lean (Fa/-) Zucker rats. Similar somatostatin levels were found in fatty and lean animals in the hypothalamic regions previously known to contain the highest hormone levels (median eminence and arcuate, periventricular and ventromedial nuclei). The fatty animals were grossly obese and had a pronounced hyperinsulinemia.
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PMID:Somatostatin concentrations in discrete hypothalamic nuclei of genetically obese Zucker rats. 290 33

One hundred twenty-seven insulinomas from 95 cases (1 malignant and 94 benign) were studied pathologically. Thirty-six tumors (35 cases) were examined by electron microscopy. Typical beta-cell secretory granules of crystalloid-form cores and/or atypical secretory granules were discerned in all tumors examined. A new type of secretory granule, with high electron-dense crystalloid-form cores and moderate electron-dense granular substance filling the space between the core and the limiting membrane, were observed in two cases. Among 68 insulinomas (67 cases) subjected to immunocytochemical investigations with ten peptide hormones (insulin, glucagon, somatostatin, pancreatic polypeptide (PP), gastrin, motilin, secretin, vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), and neurotensin), 42 were found to be multihormonal, varying from two to four peptides secreted. The hormones contained were insulin, glucagon, PP, somatostatin, and gastrin in different combinations. One patient had hyperinsulinemia and hypergastrinemia concurrently, and two islet tumors were excised at an interval of 10 months. Both electron microscopy and immunocytochemistry confirmed the presence of beta- and alpha-cells in the first tumor, whereas the second tumor revealed only G-cells by electron microscopy, and G- and beta-cells on immunocytochemical staining. The morphologic and immunocytochemical characteristics of the insulinomas in this series are discussed.
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PMID:Insulinoma. An immunocytochemical and morphologic analysis of 95 cases. 299 37


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