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)

A case of somatostatin and pancreatic polypeptide (PP) producing tumor of the pancreas is presented. A 65-year-old woman was admitted for the evaluation of the tumor in the right upper quadrant of the abdomen. Clinical abnormalities included diabetic glucose intolerance, pancreatic insufficiency and marked dilatation of gallbladder. Marked high concentration of plasma PP and low levels of plasma insulin and glucagon were observed before operation. Plasma insulin concentrations in response to oral glucose tolerance test and arginine infusion were markedly low. A large quantity of somatostatin (4,300 ng/g ww) as well as PP (1,340 ng/g ww) was detected in the tumor, and somatostatin cells and PP cells were determined by immunofluorescence studies. After operation, pancreatic insufficiency and glucose intolerance were improved, and the patient made a favorable progress.
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PMID:Somatostatinoma syndrome accompanied by overproduction of pancreatic polypeptide. 614 97

The pancreases of 17 patients who had cystic fibrosis with and without diabetes mellitus were evaluated at autopsy by routine staining and immunohistochemical methods for insulin, glucagon, somatostatin, and pancreatic polypeptide. Qualitative assessment of the number of islets of Langerhans and the degrees of exocrine pancreatic atrophy, fibrosis, and fat replacement was made for each pancreas. Quantitative assessment of islet composition was performed in 15 of the 17 based on the immunochemical reactivity of each cell type. Nondiabetic patients with cystic fibrosis in the latter part of the first decade of life have classic fibrocystic changes of the pancreas, with some persisting exocrine tissue, islets that appear normal, and prominent nesidioblastosis. The latter process may protect these patients from glucose intolerance. Young adult diabetic patients with cystic fibrosis have total loss of exocrine pancreas with fat replacement, lack of nesidioblastosis, a qualitative decrease in the number of islets, fibrosis of and amyloid deposits in islets, decreased numbers of insulin-containing cells in each islet, and atrophy of islet cells, probably resulting from progressive ischemia. Although the potential exists for an increasing incidence of diabetes mellitus in patients with cystic fibrosis as their life spans increase, individual variation occurs in this disease.
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PMID:Endocrine pancreas in cystic fibrosis: an immunohistochemical study. 636 38

Treatment of pregnant rats with cyproheptadine during the last 8 days of gestation produced alterations in the function of the endocrine pancreas in the offspring. The abnormalities exhibited by 50-day-old progeny of drug-treated dams included glucose intolerance, a two-fold increase in levels of insulin in the pancreas, and an accentuated response to the insulin-lowering action of cyproheptadine in the endocrine pancreas. The alterations observed in these animals were limited to the insulin-containing cells, and no change was found in the pancreatic concentrations of glucagon and somatostatin. The results are the first to demonstrate that postnatal pancreatic B-cell function can be selectively altered by prenatal exposure to an exogenous chemical.
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PMID:Alterations in rat pancreatic B-cell function induced by prenatal exposure to cyproheptadine. 637 61

Recent evidence suggests that the postprandial hyperglycaemia in impaired glucose tolerance is primarily due to impaired suppression of basal hepatic glucose output. This in turn appears to be secondary to decreased first phase insulin secretion, although decreased hepatic insulin sensitivity, which is a feature of non-insulin-dependent diabetes mellitus, might also play a role. Eight mildly overweight subjects with impaired glucose tolerance and eight closely matched control subjects with normal glucose tolerance underwent an intravenous glucose tolerance test to assess first phase insulin secretion. Insulin sensitivity was examined by a 150-min hyperinsulinaemic-euglycaemic clamp. Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. Glucose with added dideuterated glucose (labelled infusion technique) was infused to maintain euglycaemia. First phase insulin secretion (delta 0-10 min insulin area divided by delta 0-10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2-19.4] vs 9.1 [2.6-14.5] mU.mmol-1; p < 0.01). During the clamp, circulating insulin (93 +/- 8 [mean +/- SEM] and 81 +/- 10 mU.l-1) and glucagon (54 +/- 4 and 44 +/- 6 ng.l-1) levels were comparable. Total glucose disposal was decreased in subjects with impaired glucose tolerance (2.78 +/- 0.27 vs 4.47 +/- 0.53 mg.kg-1.min-1; p < 0.02), and was primarily due to decreased non-oxidative glucose disposal. However, hepatic glucose output rates were comparable during the clamp (0.38 +/- 0.10 and 0.30 +/- 0.18 mg.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral and hepatic insulin sensitivity in subjects with impaired glucose tolerance. 767 92

Two patients with enterocutaneous fistulas (ileal and duodenal) were successfully treated with bowel rest, total parenteral nutrition and the somatostatin analogue octreotide (150 micrograms.day-1 and 300 micrograms.day-1 respectively). At the time octreotide was started the first patient had a high output fistula (1 000 mL.day-1), the second had a low output fistula (120 mL.day-1). Within 24 hours of treatment, a reduction of at least 40% of the output was observed. The time intervals to fistula closure were respectively 6 days and 10 days after initiation of octreotide therapy. Glucose intolerance was not observed. The efficacy of octreotide combined with total parenteral nutrition supports its routine use instead of somatostatin, more expensive, less tolerated and presenting the risk of rebound effect.
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PMID:[Value of octreotide in the treatment of postoperative enterocutaneous fistula]. 773 26

The effects of two synthetic progestins, medroxyprogesterone acetate (MPA) and proligestone (PROL), on the release of growth hormone (GH) and glucose metabolism were studied in two groups of eight ovariohysterectomized dogs. Eight injections of long-acting progestins were administered at 3-week intervals. Recovery was studied in four dogs of each treatment group in the 6 months following cessation of progestin administration. Treatment with both MPA and PROL resulted in similar increases in plasma levels of GH and insulin-like growth factor I (IGF-I). The GH responses to both clonidine and growth hormone-releasing hormone became impaired. In neither treatment group did the elevated plasma GH levels decrease after administration of the synthetic somatostatin analogue SMS 201-995. The size and shape of the pituitary gland were not changed by progestin treatment. After cessation of progestin administration, basal plasma levels of GH and IGF-I did not return to pretreatment values. The GH response to growth hormone-releasing hormone remained impaired for at least 6 months after the last progestin administration. In both treatment groups, glucose homeostasis was sustained initially by increased insulin production. Prolonged treatment with MPA and PROL resulted in glucose intolerance. No amelioration was observed during the recovery period in either group. A small number of dogs developed diabetes mellitus. In more than 50% of the dogs in both treatment groups small mammary tumours developed. The recently discovered local production of GH probably played a role in mammary tumorigenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progestin treatment in the dog. I. Effects on growth hormone, insulin-like growth factor I and glucose homeostasis. 792 Dec 31

The site of impaired glucose uptake in cirrhosis is uncertain. We therefore performed hyperglycemic clamps (glucose 10 mmol/L) in 10 patients with compensated alcoholic cirrhosis and impaired glucose tolerance and in six control subjects. Muscle glucose uptake was estimated in patients and controls with the forearm technique. In the cirrhotic subjects splanchnic glucose uptake was measured with hepatic vein catheterization and primed continuous infusions of indocyanine green and [6-3H]glucose. To assess insulin-independent glucose uptake and the effects of elevated nonesterified fatty acid levels on glucose uptake, we repeated the study with somatostatin to induce insulin deficiency and a nicotinic acid analog, acipimox, to inhibit lipolysis. Substrate disposal was assessed on indirect calorimetry. Despite similar stimulated insulin levels, total glucose utilization was lower in the cirrhotic subjects (3.9 +/- 0.3 vs. 8.8 +/- 1.7 mg/kg/min, p = 0.006). This deficiency was accounted for by lower nonoxidative glucose disposal (1.2 +/- 0.2 vs. 5.8 +/- 1.6 mg/kg/min, p = 0.002). Forearm glucose uptake was lower in the cirrhotic subjects (0.39 +/- 0.06 vs. 1.21 +/- 0.3 mg/100 ml/min, p = 0.001). However, splanchnic glucose uptake at 1.59 +/- 0.14 mg/kg/min was similar to that reported in other studies of normal subjects. Insulin-independent glucose uptake was normal, and acipimox had no effect on total or forearm glucose utilization. Glucose intolerance in cirrhosis is characterized by impaired peripheral insulin-stimulated non-oxidative glucose disposal. The high nonesterified fatty acid levels seen in cirrhosis most likely do not contribute to this defect. Splanchnic glucose uptake is normal in cirrhosis.
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PMID:Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis. 810 Jul 99

At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. We have measured their different molecular forms in plasma of six female controls, six normal pregnant (NP) women and six gestational diabetic (GD) women under basal conditions and 30 min after an oral glucose load (100 g) and a liquid mixed meal in order to study if their alteration could contribute to the impaired glucose tolerance in GD. Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. Neurotensin-1-13 was the main molecular form of all neurotensins at basal time in the three groups studied, being higher in GD in comparison with controls and NP. Somatostatin-1-14 was the predominant molecular form in controls and GD under basal conditions and did not show any change any change after stimuli. In NP, somatostatin-1-14 showed a significant increase following both kinds of stimuli. Total gastrin concentrations in NP and GD showed a significant increase after the glucose load, which was not observed in controls. Gastrin-17 was the main molecular form at basal time and 30 min post-stimuli in GD but not in NP and controls. We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. 810 15

In Taipei, Taiwan, physicians started 13 normally menstruating women on an isocaloric diet (30 kcal/kg; 50% carbohydrate, 30% fat, and 20% protein) and administered a combined triphasic oral contraceptive (OC) to evaluate the effect of the OC on insulin resistance and lipid metabolism including Lp(a) values. (Lp(a) levels may be a risk factor for coronary heart disease.) After three months of taking OCs, the plasma glucose concentration increased significantly (p 0.05). The plasma insulin response to oral glucose was also significantly higher than before OC use (p 0.03). The steady state plasma glucose concentration during constant infusion of glucose, insulin, and somatostatin was much higher three months after OC administration than before OC administration (12.4 vs. 7.5 mmol/l; p 0.001). After three cycles of OC use, the only fasting plasma lipoprotein that increased significantly was triglyceride (0.81 vs. 1.09 mmol/l; p 0.03). The Lp (a) levels stayed essentially the same. OC use decreased significantly the concentration of all serum steroids except DHEAS. These findings indicate that administration of a triphasic low dose OC for three cycles caused glucose intolerance, hyperinsulinemia, and insulin resistance in normal women. It also raised plasma triglyceride concentrations, but did not affect Lp(a) and other lipid values.
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PMID:Prospective evaluation of insulin resistance and lipid metabolism in women receiving oral contraceptives. 813 25

To determine the effect of the somatostatin analog octreotide on glucose tolerance in acromegaly, we examined glucose profiles, oral glucose tolerance and the insulinogenic index in patients treated with this analog. Ninety patients participated in a long-term, prospective, open-label study. There was no significant change between mean daily blood glucose profiles at baseline or during octreotide treatment. Using glucose tolerance test criteria, 61% of 90 patients had normal baseline glucose tolerance. While on octreotide, 20% and 29% of these patients, respectively, developed impaired glucose tolerance or became frankly diabetic. Conversely, three of the patients who were diabetic at baseline (N = 11) became normal (18%) or developed impaired glucose tolerance (9%) during octreotide therapy. There was no relationship between the dose of octreotide and change in glycemic state. The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Female patients and those with elevated baseline insulin levels were more likely to develop diabetes mellitus during octreotide therapy. In conclusion, octreotide significantly alters glucose tolerance in patients with acromegaly, mandating glucose monitoring during this form of therapy.
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PMID:Effect of octreotide on glucose tolerance in acromegaly. 820 58


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