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)

In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Although the principal tissue sites for IMGU are skeletal muscle, the tissue sites for NIMGU at a given serum glucose concentration are not known. To examine this issue, rates of whole body glucose uptake (Rd) were measured at basal and during glucose clamp studies performed at euglycemia (approximately 90 mg/dl) and hyperglycemia (approximately 220 mg/dl) in six lean healthy men. Studies were performed during hyperinsulinemia (approximately 70 microU/ml) and during somatostatin-induced insulinopenia to measure IMGU and NIMGU, respectively. During each study, leg glucose balance (arteriovenous catheter technique) was also measured. With this approach, rates of whole body skeletal muscle IMGU and NIMGU can be estimated, and the difference between overall Rd and skeletal muscle glucose uptake represents non-skeletal muscle Rd. The results indicate that approximately 20% of basal Rd is into skeletal muscle. During insulinopenia approximately 86% of body NIMGU occurs in non-skeletal muscle tissues at euglycemia. When hyperglycemia was created, whole body NIMGU increased from 128 +/- 6 to 213 +/- 18 mg/min (P less than 0.01); NIMGU into non-skeletal muscle tissues was 134 +/- 11 and 111 +/- 6 mg/min at hyperglycemia and euglycemia, respectively, P = NS. Therefore, virtually all the hyperglycemia induced increment in NIMGU occurred in skeletal muscle. During hyperinsulinemia, IMGU in skeletal muscle represented 75 and 95% of body Rd, at euglycemia and hyperglycemia, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humans. 305 16

Five infants with hypoglycaemia due to hyperinsulinism were treated for between three and 11 days with a somatostatin analogue, which raised the mean blood glucose concentration and lowered the glucose requirements in all. Somatostatin analogue appears to be useful in the short term management of these patients.
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PMID:Somatostatin analogue in short term management of hyperinsulinism. 323 99

Eight hyperthyroid and eight normal subjects underwent 2-h oral glucose tolerance tests (OGTT) and euglycemic clamp studies to assess the presence of peripheral and hepatic insulin antagonism in hyperthyroidism. Although the mean total glucose area during the OGTT was similar in the hyperthyroid patients and normal subjects [16.4 +/- 0.8 (+/- SE) vs. 15.8 +/- 0.7 mmol/L.h], the mean insulin area was significantly elevated in the hyperthyroid group (1413 +/- 136 vs. 1004 +/- 122 pmol/L.h; P less than 0.05). Basal hepatic glucose production was measured during the second hour of a primed [3-3H]glucose infusion. A two-insulin dose euglycemic clamp study with [3-3H]glucose and somatostatin (500 micrograms/h) was carried out during the next 6 h. The insulin infusion rate was 0.05 mU/kg.min during the third, fourth, and fifth hours and 0.60 mU/kg.min during the sixth, seventh, and eighth hours. Hepatic glucose production and glucose utilization were measured during the final 0.5 h of each clamp period. Serum C-peptide concentrations were measured in the initial sample and in the last sample of each clamp period. The mean equilibrium serum insulin concentrations were similar in both groups during the final 0.5 h of the low (90 +/- 8 vs. 79 +/- 6 pmol/L) and high (367 +/- 11 vs. 367 +/- 15 pmol/L) insulin infusion rates. Basal serum C-peptide levels were significantly increased in the hyperthyroid patients (596 +/- 17 vs. 487 +/- 43 pmol/L; P less than 0.05) but were suppressed equally in both groups at the end of both clamp periods. The MCRs of insulin were similar in the hyperthyroid and normal subjects during the low (6.7 +/- 1.1 vs. 5.6 +/- 0.5 mL/kg.min) and high (11.9 +/- 0.4 vs. 12.1 +/- 0.5 mL/kg.mm) insulin infusion rates. Glucose production was significantly increased in the hyperthyroid patients during the basal state (17.6 +/- 0.9 vs. 11.5 +/- 0.5 mumol/kg.min; P less than 0.001) and remained elevated during the final 0.5 h of the low (12.1 +/- 1.1 vs. 5.9 +/- 1.7; P less than 0.01) and high (3.2 +/- 1.2 vs. 0.5 +/- 0.3; P less than 0.05) insulin infusion rates. Peripheral insulin action, assessed by Bergman's sensitivity index, was significantly decreased in the hyperthyroid patients (7.4 +/- 2.2 vs. 15.6 +/- 2.1 L/kg min-1/pmol/L; P less than 0.02). In conclusion, hyperthyroidism is characterized by 1) hyperinsulinemia after oral glucose loading, 2) increased basal hepatic glucose production, 3) impairment of insulin-mediated suppression of hepatic glucose production, and 4) antagonism to insulin-stimulated peripheral glucose utilization.
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PMID:Peripheral and hepatic insulin antagonism in hyperthyroidism. 328 May 88

To investigate the difference of insulin action between skeletal muscle and adipose tissue in response to dietary manipulation, we studied the effect of high-sucrose (HS) and high-fat (HF) diet on insulin action by measuring insulin binding and insulin action both in soleus muscles and adipocytes. HS feeding led to a 14 and 28% decrease, and HF feeding led to a 25 and 36% decrease in insulin binding both to soleus muscles and adipocytes, respectively (P less than 0.01). In HF-fed rats, both rates of glucose uptake and intracellular glucose metabolism were impaired by 30-40% in soleus muscles (P less than 0.01), and adipocyte glucose uptake was also decreased by 30% in the submaximally insulin-stimulated state (P less than 0.05). On the other hand, in HS-fed rats with prominent hyperinsulinemia, glucose uptake was 2.3- to 2.7-fold increased in adipocytes (P less than 0.01). However, both rates of glucose uptake and intracellular glucose metabolism were not increased in soleus muscles from HS-fed rats. Steady-state plasma glucose (SSPG) level was unchanged in HS-fed rats during somatostatin, glucose, and insulin infusion, whereas the SSPG level of HF-fed rats was twice as much as that in controls (P less than 0.01). These results indicate that long-term regulation of glucose metabolism by ambient insulin in skeletal muscle may be different from that in adipocytes and that insulin action in muscle, rather than in adipocyte, may reflect insulin action of whole body.
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PMID:Effect of diet change on insulin action: difference between muscles and adipocytes. 353 36

The authors have studied insulin receptors on peripheral blood monocytes and insulin sensitivity, evaluated by simultaneous infusion of glucose, insulin and somatostatin in 10 control subjects and in 20 obese patients with normal glucose tolerance. The obese patients have been divided into two groups, normo (NO) and hyperinsulinemic (HO), according to the total insulin response during OGTT. We considered HO patients with insulin response higher than M + 2DS of controls. Obese patients showed, in comparison to the controls, a lower specific binding and higher degree of insulin resistance. The subdivision of obese patients allowed us to distinguish two groups. The first was characterized by basal hyperinsulinemia, normal insulin response to the stimulus, reduced number of insulin receptors and normal or slightly reduced sensitivity. The second group showed high basal and after stimulus insulinemic values, reduced number of insulin receptors and high level of insulin resistance. When we compared the two groups of obeses we found that the first has a shorter duration of obesity and lower blood glucose values after OGTT. However both groups show the same reduction of insulin bound and the same degree of basal hyperinsulinemia. These data suggest that a reduction of insulin receptors is not the main factor responsible for insulin resistance in obesity. Furthermore, the presence of basal hyperinsulinemia and normal insulin sensitivity in our first group suggests that the modification of basal insulin concentrations is not dependent on the presence of insulin resistance.
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PMID:Insulin receptors and insulin sensitivity in normo and hyperinsulinemic obese patients. 389 56

Previously, we reported that pancreatic acini have specific receptors for the insulin-like growth factors (IGF) I and II. We now report that the binding of 125I-labeled IGF II to mouse pancreatic acini is maximally increased by 100 nM insulin (51%) and is maximally reduced by 10 nM cholecystokinin octapeptide (CCK8) (34%), but is not affected by other regulatory peptides such as somatostatin or glucagon. Since many polypeptide hormones are internalized, we determined whether this regulation of IGF II binding occurred via a change in internalization. Acid washing or trypsinization has been shown to remove surface-bound hormone while the acid- or trypsin-resistant radioactivity represents internalized radioligand. Insulin increased and CCK8 decreased the internalization of IGF II as determined by these techniques. Studies of IGF II binding to acini at low temperature (15 degrees C) and binding to particulate fractions from acini were also consistent with the effect of insulin to increase and CCK8 to decrease the internalization of IGF II. When insulin and CCK8 were added together, the inhibitory effect of CCK8 predominated, indicating that CCK8 acted distal to the effect of insulin. Several lines of evidence suggest that this effect of CCK8 was via the CCK receptor and was mediated via a change in intracellular Ca2+: the effect of CCK8 on inhibiting IGF II binding was blocked by the cholecystokinin antagonist N2,O2'-dibutyryl cGMP; the cholinergic agent carbachol (1-100 microM), which acts through the muscarinic receptor to increase intracellular Ca2+, also inhibited IGF II binding; the Ca2+ ionophore A23187 (1-5 microM) mimicked the effects of CCK8 and carbachol. These data indicate, therefore, that CCK8 and possibly insulin may regulate the internalization of IGF II via intracellular Ca2+. Moreover, the data raise the possibility that alterations of hormone internalization may be a general phenomenon of hormone-hormone interaction.
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PMID:Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin. 609 32

Two patients with somatostatin-secreting pancreatic tumours are described, one presenting with hypoglycaemia due to hyperinsulinism, and the other with Cushing's syndrome due to ectopic ACTH production. When plasma from these patients was subjected to gel chromatography under conditions designed to prevent somatostatin binding to larger proteins, a peak of monomeric immunoreactive somatostatin was observed as well as several large molecular weight forms. These larger forms of somatostatin could be dissociated into monomeric somatostatin by dithiothreitol. Similar studies on plasma obtained from normal subjects also showed heterogeneity of circulating somatostatin. Extracts of tumour tissue from both patients contained predominantly monomeric somatostatin, but only small amounts of high molecular weight somatostatin which differed from the profile seen in plasma. The site(s) of origin of the large molecualr weight forms of somatostatin seen in plasma and their relative biological activities remain to be established.
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PMID:Molecular forms of somatostatin in normal subjects and in patients with pancreatic somatostatinoma. 610 27

Somatostatin-like immunoreactivity (SRIF-LI) content in 2 N acetic acid extracts of hypothalamus, gastric antrum, and pancreas was measured in genetically obese (C57BL/6J ob/ob and db/db) and diabetic (C57BL/KsJ db/db and ob/ob) mice and normal littermate controls from 5 to 24 wk to determine the relationship of previously reported changes to the development of metabolic abnormalities. Hypothalamic SRIF-L concentration was similar in control, diabetic, and obese mice at all ages and increased progressively with age in all groups. Gastric antrum SRIF-LI was similar in all groups of mice at all ages. Obese mice gained weight progressively and showed moderate hyperglycemia and marked hyperinsulinemia from 5 wk of age. Pancreatic SRIF-LI content in obese (C57BL/6J) animals was similar to that in lean littermate controls, but pancreatic SRIF-LI concentration (expressed by weight or protein content) was decreased until 8 (6J ob/ob) and 10 (6J db/db) wk. Diabetic (C57BL/KsJ) mice showed a similar metabolic pattern until 10 wk with no change in pancreatic SRIF-LI content or concentration. Thereafter a progressive fall in serum insulin and a marked rise in serum glucose was associated with increasing pancreatic SRIF-LI content and concentration. These studies suggest that the genetically hyperphagic syndromes are unassociated with any change in hypothalamic or gastric SRIF-LI; that pancreatic SRIF-LI increases occur in response to, rather than as the cause of, relative hypoinsulinemia; and that the genetic background of the mice (KsJ or 6J) rather than the mutant gene (db or ob) determines the defect in carbohydrate metabolism and the pancreatic SRIF-LI response.
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PMID:Temporal relationship of tissue somatostatin-like immunoreactivity to metabolic changes in genetically obese and diabetic mice. 610 73

Qualitative and quantitative immunocytochemistry, electronmicroscopy and radio-immuno-assays led to the discovery of 5 pancreatic polypeptide hormones under physiological conditions. The active endocrine cells and the produced hormones are termed A, B, D, D1, and PP cell and glucagon, insulin, somatostatin, vasoactive intestinal polypeptide (VIP) and pancreatic polypeptide (PP) respectively. Beside the physiology of secretion and action a survey of pathological conditions in the paediatric age group is given. Insulin is the most important of pancreatic hormones in childhood. Therefore diagnosis and treatment of hyperinsulinism are described in extension.
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PMID:[Physiology and disease of the endocrine function of the pancreas (author's transl)]. 610 37

The inappropriate insulin release that is characteristic of severe neonatal hypoglycemia and nesidioblastosis was thought to be principally due to a marked proliferation of B-cells. A possible deficiency of somatostatin, one of the factors controlling insulin release, has only recently been considered. We report have a significant decrease of pancreatic somatostatin cells and somatostatin content in nesidioblastosis, as compared with appropriate controls. Pancreatic tissue from five babies with severe hypoglycemia, hyperinsulinemia, and nesidioblastosis was examined for insulin, somatostatin, and glucagon by immunocytochemistry and radioimmunoassay. There was a variable insulin cell hyperplasia among the nesidioblastotic specimens but no significant difference from controls was detected. In contrast, there was a consistent and highly significant (P less than 0.02) decrease (of more than 50%) of somatostatin cells (controls, 1.29 +/- 0.22%; nesidioblastosis, 0.53 +/- 0.14%, mean +/- SEM). Similarly, there was no significant alteration in insulin content, although a slight increase was found in non-microadenomatous areas of the diseased pancreata (controls, 42.3 +/- 4.1; nesidioblastosis, 58.6 +/- 9.4 nmol/g wet weight of tissue, mean +/- SEM). However, somatostatin content was almost 60% below control values (controls, 0.365 +/- 0.038; nesidioblastosis, 0.16 +/- 0.039 nmol/g), a statistically significant difference (P less than 0.01). Thus, a marked reduction in the content of somatostatin was present in the pancreata of these infants with nesidioblastosis, resulting in a distinct alteration of the normal pancreatic hormone balance.
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PMID:Decrease of pancreatic somatostatin in neonatal nesidioblastosis. 611 May 95


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