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)

Insulin, glucagon, somatostatin and pancreatic polypeptide cells were quantified after immunoperoxidase staining in sections of pancreases obtained from nine control subjects and seven diabetic patients with primary or secondary iron overload. One was normoglycaemic, two had glucose intolerance and four presented insulin-requiring diabetes. The whole pancreas was studied, taking into account the heterogeneous distribution of the endocrine cells. In the diabetic patients, the weight of the pancreas tended to be lower. Iron overload predominated in the exocrine tissue, whereas in islets iron concentration was quite variable from case to case. At the Haemalun-Eosine staining the histological appearance of the islets was normal, their shape and size being unchanged; amyloid deposits were absent, as were atrophic islets. Immunoperoxidase staining revealed a severe reduction in the number of immunoreactive B cells in the four diabetic patients. The mass of immunoreactive B cells was calculated from their volume density and from the weight of each lobe of the pancreas. It averaged 950 mg in control subjects, 1580 mg in the normoglycaemic patient, 1010 mg in patients with glucose intolerance and 180 mg in insulin-requiring diabetic patients. The electron microscopic examination, performed in four cases, revealed that the iron deposits were restricted to B cells and associated with progressive loss of their endocrine granules. The study shows that the pancreatic islet abnormalities in iron overloaded diabetic patients are completely different from those of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients. This constitutes a further argument for a specific role of iron in the pathogeny of diabetes in haemochromatotic patients.
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PMID:The haemochromatotic human pancreas: a quantitative immunohistochemical and ultrastructural study. 355 22

The endocrine pancreas of birds contains 3 islet types and releases glucagon, insulin, somatostatin and avian pancreatic polypeptide (APP). Interactions between these hormones, and pancreatic hormone-plasma metabolite feedback mechanisms, are the main regulators of these secretions. In birds, total pancreatectomy induces a fatal hypoglycaemia associated with the disappearance of circulating glucagon, and an impaired glucose tolerance ascribed to the lack of insulin. Normoglycaemia can be restored in depancreatized birds by infusion of glucagon and insulin, provided that the G/I ratio is close to normal. Subtotal pancreatectomy provokes a diabetes characterized by a basal hyperglycaemia and an impaired glucose tolerance. However, while a transient diabetes is observed in most species, in the goose a permanent diabetes is obtained. These results point out the importance of the pancreas and especially of glucagon, in birds. This importance can also be detected in the protein metabolism, since total or subtotal pancreatectomy markedly increases the concentration of plasma aminoacids. As for lipid metabolism, in vivo and/or in vitro experiments have shown the sensitivity of the adipose tissue and liver cells to glucagon. Finally, contrary to the general opinion, insulin seems to be antilipolytic, as in mammals.
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PMID:[The endocrine pancreas of birds]. 610 57

Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. To determine whether the insulin resistance of glucose-intolerant obese subjects can be accounted for by obesity alone, insulin-mediated glucose disposal was measured in 14 glucose-intolerant and 21 nondiabetic. Southwestern American Indians with similar degrees of obesity. A mixture of insulin, glucose, and somatostatin was infused which delivered the same quantity of glucose and achieved similar plasma insulin concentrations in all subjects. Despite similar steady state plasma insulin levels, the mean steady state plasma glucose concentration was higher in the glucose-intolerant subjects than in weight-matched subjects with normal glucose tolerance (226 +/- 10 vs. 136 +/- 13 mg/dl; P < 0.0001). This increased resistance to insulin action was found in the presence of similar insulin binding to mononuclear cells (measured in 8 glucose-intolerant subjects and 9 subjects with normal glucose tolerance). In obese Southwestern American Indians with glucose intolerance, abnormalities beyond the site of insulin binding to its receptor may explain the observed increase in in vivo insulin resistance.
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PMID:Increased insulin resistance in obese, glucose-intolerant Southwestern American Indians: evidence for a defect not explained by obesity. 610 47

Islets of 5-mo-old obese Zucker rats secreted 50% more somatostatin (SRIF) in response to 8.3 mM or 16.7 mM glucose than did islets from lean controls; the islet SRIF contents of obese and lean rats were similar. As expected, islets of obese rats demonstrated a greater basal and a fivefold greater glucose-induced insulin release and also a twofold greater insulin content than did islets from lean rats. Obese rats were pair fed with lean animals from the age of 9 wk until killed, when 5 mo old. While this curtailed the weight gain of obese rats to that of lean controls, it caused no reduction in the percent body weight found in the form of lipid. The responses of the pancreatic delta and beta cells to pair feeding were markedly different. Pair feeding caused no alteration in either SRIF content or glucose-induced SRIF release, while the expected reductions in both islet insulin content and glucose-induced insulin secretion were observed. Islets from older obese Zucker rats (15--18 mo old) had four to five times greater contents of both SRIF and insulin than did islets from age-matched lean controls. The obese rats of this age had a moderate glucose intolerance. SRIF secretion from the islets of such rats was distinctly greater than from those of lean controls at all glucose concentrations tested (range, 1.0--16.7 mM). The delta cells of the older obese rats had lost their sensitivity to glucose, while those of lean controls remained sensitive. Beta cells of islets from both obese and lean 15-mo-old rats remained glucose sensitive. Under all conditions tested, secretion of SRIF and insulin was greater from islets of obese than lean rats. The results demonstrate a marked difference in pancreatic delta and beta cell responses to pair feeding in the obese Zucker rat. At present, the role played by hypersecretion of pancreatic SRIF in the obesity syndrome of the Zucker rat remains obscure.
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PMID:Hypersection of pancreatic somatostatin in the obese Zucker rat: effects of food restriction and age. 610 55

Previous evidence has documented the hyperglycemia and glucose intolerance that occur during prolonged infusions of somatostatin and in patients with somatostatinoma. We studied glucose utilization and production and gluconeogenesis (from alanine) in a patient with the somatostatinoma syndrome (peripheral somatostatin levels 20,000 pg/ml) during saline (basal state) and glucose infusion (1.78 mg/kg . min). Plasma glucose levels increased from 163 to 229 mg/100 ml during glucose infusion, whereas lactate, free fatty acid, and glucagon levels did not change. Endogenous glucose production decreased from 7.34 to 0.0 mumol/kg . min, and the percentage of glucose derived from alanine also decreased from 10.5 to 7.4. Glucose clearance decreased from 0.81 to 0.74 cc/kg . min and suggests that the hyperglycemia of the somatostatinoma syndrome is secondary to reduced peripheral glucose utilization secondary to relative insulin deficiency.
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PMID:Glucose turnover and gluconeogenesis in a patient with somatostatinoma. 611 Feb 46

Insulin sensitivity has been determined in primary nonobese diabetics and subjects with borderline glucose intolerance by a newly devised technique using glucose, insulin, and somatostatin infusion. Insulin sensitivity for glucose utilization was decreased in both adult- and juvenile-onset diabetics. Eight out of 88 diabetics had normal insulin sensitivty and were free from microvascular complications. In lean subjects with borderline glucose intolerance, insulin sensitivity was decreased, although an overlap with normal was noted. All obese subjects with borderline glucose intolerance had reduced insulin sensitivity. An inverse relationship was observed between insulin sensitivity and fasting plasma glucose (FPG), and a significant correlation was observed between FPG and steady state plasma glucose levels (SSPG; r = 0.57; P less than 0.001). Improvement of diabetic control in eight diabetics with sulfonylureas decreased SSPG in all (P less than 0.05), although normalization of SSPG was observed in only one. These results indicate that decreased sensitivity of insulin for peripheral glucose utilization may play an important role in the pathogenesis of diabetes. Elevated FPG levels reflect the presence of decreased insulin sensitivity in diabetes mellitus. Although decreased sensitivity is difficult to normalize, it can be enhanced by improving the diabetic control. An effort to maintain or enhance tissue insulin sensitivity in diabetes mellitus may be more important than attempts to stimulate the deteriorating pancreatic beta-cells to secrete more insulin.
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PMID:Clinical significance of altered insulin sensitivity in diabetes mellitus assessed by glucose, insulin, and somatostatin infusion. 611 34

Insulin resistance was studied in seven non-obese male subjects with impaired glucose tolerance and four healthy, age and body-weight matched male control subjects by means of a continuous intravenous infusion of somatostatin, glucose and insulin over 150 min. Glucose tolerance was evaluated by means of a 2-h glucose infusion test. Endogenous insulin (C-peptide), growth hormone, and glucagon secretion were suppressed by somatostatin in both groups. Steady-state plasma insulin and glucose levels were achieved between 90-135 min. Since similar steady-state levels of exogenous insulin were achieved, the resulting steady-state plasma glucose level provided a direct estimate of the ability of insulin to dispose of the infused glucose. The glucose levels were higher in subjects with impaired glucose tolerance with values of 14.6 +/- 1.8 mmol/l compared with 5.1 +/- 1.2 mmol/l in control subjects (p less than 0.01), thus indicating insulin resistance. There was a direct correlation between the steady-state plasma glucose level and glucose tolerance suggesting that the degree of glucose intolerance is proportional to the degree of insulin resistance. These results revealed that decreased insulin sensitivity is found in non-obese subjects with impaired glucose tolerance.
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PMID:Evaluation of insulin resistance during inhibition of endogenous insulin and glucagon secretion by somatostatin in non-obese subjects with impaired glucose tolerance. 611 92

The effect of subtotal pancreatectomy on the regulation of plasma glucose was studied in the chicken. The eventual appearance of an extra-pancreatic source of insulin and the effect of pancreatectomy on somatostatin containing cells of the intestine were also investigated. Over a period of 3-5 weeks, pancreatectomy decreased body weight gain, greatly impaired glucose tolerance and hindered the regulation of plasma glucose levels after a meal. A large deficit in the insulin release induced by a meal was noticed after pancreatectomy. Therefore, in the fed chicken, pancreatectomy results in the typical signs of diabetes. No extrapancreatic source of insulin could be found either by radioimmunoassay of extracts of proventriculus, gizzard, gizzard-duodenum junction and duodenum from controls or depancreatized chickens, or by immunohistological studies in the same organs plus pancreatic ducts. No glucagon producing cells could be found by immunohistological studies in the gastrointestinal tract. The size of the somatostatin cells from the gizzard-duodenum junction was negatively related to the magnitude of the glucose-induced insulin release, which suggests an increase in somatostatin cell activity in true insulin-deficient depancreatized chickens as observed in insulin deficient diabetic mammals.
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PMID:Subtotal pancreatectomy in the chicken: evidence of a diabetic state and effect on the somatostatin cells of the digestive tract. 613 85

The aim of the present study was to evaluate the insulin and glucagon responses to various stimuli in patients following pancreatic transplantation. Four Type 1 (insulin-dependent) diabetic patients with end-stage renal failure who had received a cadaveric segmental, neoprene-injected, pancreas transplant, in association with kidney transplantation, were investigated. Free-insulin, pancreatic glucagon, and growth hormone concentrations were measured after both oral and intravenous glucose tolerance tests, and following tolbutamide, arginine and arginine plus somatostatin infusions. Tests were performed 1 month (three cases) and 30 months (one case) after surgery, when no insulin administration was required. Four non-diabetic kidney grafted patients, matched for duration of graft survival and immunosuppressive treatment (steroids, azathioprine and anti-lymphocyte-globulins), served as control subjects. Impaired glucose tolerance was present in all diabetic and control patients. This was possibly related to immunosuppressive treatment. In comparison with control subjects, insulin release was normal in response to arginine and tolbutamide but was reduced in response to oral and intravenous glucose, while glucagon and growth hormone release were similar in both groups. Somatostatin was less effective in diabetic patients than in control subjects in suppressing insulin and glucagon release.
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PMID:Endocrine responses of type 1 (insulin-dependent) diabetic patients following successful pancreas transplantation. 613 51

To study the role of somatostatin in the pathophysiology of glucose intolerance in man, plasma somatostatin-like immunoreactivity (SLI) was measured in 8 normal subjects, 6 patients with insulin dependent diabetes mellitus (IDDM), 13 with non-insulin dependent diabetes mellitus (NIDDM), and 9 with hyperthyroidism, by extraction of plasma SLI and radioimmunoassay. The extraction method gave a recovery rate for synthetic somatostatin-14 and somatostatin-28 of 72 +/- 6 and 55 +/- 7%, respectively. No SLI corresponding to somatostatin-28 in human peripheral blood was observed. Incubation of somatostatin-28 in plasma gave a rapid decrease of immunoreactivity, and no conversion to somatostatin-14 was observed. It is speculated that SLI extracted with acid-acetone mainly represents a molecular weight similar to somatostatin-14. After oral administration of glucose (75 g), a clear and sustained rise in plasma SLI was seen in normal subjects from an initial value (+/- SEM) of 29.9 +/- 5.4 pg/ml to a peak value, at 60 min of 93.4 +/- 15.5 pg/ml. The increase of plasma SLI after 75 g glucose was also observed in IDDM and NIDDM. The peak level of SLI was significantly less than that for normal subjects. The extraction of plasma SLI with acetic acid and acetone gave reproducible results and showed a fluctuation of SLI with glucose concentration.
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PMID:Response of plasma somatostatin-like immunoreactivity (SLI) to a 75 g oral glucose tolerance test in normal subjects and patients with impaired glucose tolerance. 614 Aug 6


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