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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay (RIA) method for somatostatin (SRIF) utilizing rabbit antiserum against synthetic SRIF coupled with human serum alpha-globulin is described. Synthetic N alpha-tyrosylated SRIF was labelled with 125I using the lactoperoxidase method and purified on a Sephadex G-10 column. This assay system was highly specific for SRIF and did not cross-react with hypothalamic trophic hormones, pituitary trophic hormones or gastrointestinal hormones. The effect of streptozotocin induced diabetes on the SRIF content was examined in the pancreas, the pancreatic islets, as well as the hypothalamus of rats. SRIF content in both the pancreas and islets of the diabetic rats was shown by RIA to have significantly increased. However, content in the hypothalamus of the diabetic rats did not differ from that of the control. The physiological and pathophysiological significance of the SRIF changes remains to determined.
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PMID:Effect of streptozotocin administration on somatostatin content of pancreas and hypothalamus in rats. 14 51

Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. Plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. Autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.
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PMID:Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia. 19 43

The functional properties of granulocytes in a diabetic patient deficient in myeloperoxidase (MPO) were compared with those of granulocytes in healthy subjects. The granulocytes of this patient had normal phagocytic activity. The microbicidal activity of the granulocytes was partially diminished with regard to Staphylococcus aureus and was almost nil with regard to Candida albicans. Fungicidal activity of normal granulocytes was shown to be impaired during the in vitro artificial hyperglycemic condition. The relationship among diabetes mellitus, MPO deficiency, and serious C. albicans infection was examined. Genetic investigation was carried out in 28 members of the proband's family. In close relatives of the patient, MPO values were found to be diminshed to a greater or lesser degree, thus suggesting variable expressivity of the heterozygote state of MPO deficiency.
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PMID:Hereditary myeloperoxidase deficiency. 21 38

The variation of the activities of glutathion peroxidase, glutathion reductase, glucose-6-phosphate dehydrogenase, as well as of the concentrations of lipid peroxides and -SH groups of nonproteic nature, was followed up in the hepatocyte of normal rats, of those with, streptozotocin-induced-diabetes, and of diabetic rats treated with thiazolidin carboxylic (ThCA) acid. Free peroxides and glutathion peroxidase were increased in the diabetic animals as against the normals, whereas glutathion reductase, glucose-6-phosphate dehydrogenase and the -SH groups of nonproteic nature had lower values. A return to normal of these parameters was noticed in the animals treated with ThCA.
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PMID:The effect of thiazolidin carboxylic acid (ThCA) on the redox equilibrium maintaining in the rat hepatocyte with streptozotocin-induced diabetes. 63 31

Increased permeability of retinal blood vessels in human diabetic retinopathy is well known clinically. Its morphologic equivalent is unknown. In dogs with 5 years of poorly controlled alloxan diabetes and nonproliferative diabetic retinopathy comparable to that of man, permeability and patency of retinal blood vessels were tested with the protein tracer horseradish peroxidase and evaluated by electron microscopy. A breakdown of the blood-retinal barrier was found associated with extensive tracer leakage around retinal blood vessels. Tracer had seemingly permeated endothial junctions, and was not transported through the endothelial cytoplasm. Blood vessels which had lost their endothelial cells and were partially occluded by glial cells retained some patency to tracer. These findings suggest the following. (1) Endothelial tight junctions are not a static cell specialization but one that can open due to chronic metabolic or osmotic factors prevailing in diabetes. Opened tight junctions may account for plasma leakage seen clinically in human diabetic retinopathy. (2) In the absence of endothelial cells perfusion does not necessarily end abruptly. The tracer method and electron microscopy may show details of vascular obstruction that are not readily demonstrated clinically.
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PMID:Permeability and patency of retinal blood vessels in experimental diabetes. 85 45

The lectin-horseradish peroxidase conjugate of GSA I-B4 (Griffonia simplicifolia isolectin) has some binding affinity with capillary walls in sections of the major salivary glands from normal rats. After inducing diabetes with streptozotocin a conspicuous increase in the staining intensity with GSA I-B4 was already evident in parotid capillaries at 3 weeks and this increase persisted at 3 and 6 months. In submandibular capillaries, however, an increased uptake of GSA I-B4 was evident only at 6 months after inducing diabetes. The reasons for these different time scales in the two glands are not known but the increased uptake of GSA I-B4, which is due to an increase in carbohydrate-containing sites with available terminal alpha-D-galactose, is considered to reflect a pathological change.
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PMID:Changes in the lectin-binding of capillaries in rat salivary glands after streptozotocin-induced diabetes. 141 25

The labelling of interleukin-2 (IL-2) with 123I and its in vivo application for imaging chronic pathological lymphocytic infiltrations are described. The lactoperoxidase/glucoseoxidase technique was the labelling method of choice leading to immunoreactive IL-2 with high specific activity. Labelled IL-2 was injected in diabetes-prone non-obese diabetic (NOD) mice with pancreatic lymphocytic infiltration. As control animals, Balb/c mice were used. As specificity control, monoclonal antibodies AMT13 and UCHT1, bovine serum albumin and alpha-lactalbumin were radioiodinated and injected in mice. Eighteen NOD mice and four control Balb/c mice were used for gamma camera imaging experiments. Fifty-four NOD and 20 Balb/c mice were used for time course single organ counting and autoradiography. Gamma camera images showed that radioactivity accumulated in the pancreatic region from the 10th minute onwards in NOD mice injected with 123I-IL-2 but not in Balb/c mice, or in NOD mice injected with control radiopharmaceuticals. These findings were confirmed by counting the radioactivity present in single organs. Autoradiography of NOD pancreas, after injection of labelled IL-2, showed that radioactivity was specifically associated with infiltrating lymphocytes. In conclusion, this technique is highly specific and easy to perform and we suggest its application in humans for in vivo detection of areas of lymphocytic infiltration.
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PMID:A radiopharmaceutical for imaging areas of lymphocytic infiltration: 123I-interleukin-2. Labelling procedure and animal studies. 149 35

The effects of long-term high-fiber diet on lipid and glucose levels and the histological changes in the coronary arteries and thoracic aorta in STZ-induced diabetic SD rats were investigated. During the first 4 weeks of the study period, all diabetic rats were given regular chow plus water after which, all were grouped according to the following diet regimen: group II, no added cholesterol and glucomannan; group III, no added cholesterol but with glucomannan supplement, group IV, with added cholesterol but no glucomannan supplement; and group V, with both cholesterol and glucomannan supplements. 15% weight of glucomannan and 1.5% weight of cholesterol in regular rat chow were used as supplements when indicated. Non-diabetic rats which received only regular chow served as the control group (group I). In the 18th week all rats were sacrificed and weight gain, glucose, total cholesterol, HDL-cholesterol, triglyceride and lipid peroxidase concentrations were determined. Selected portions of the heart and thoracic aorta were histologically examined. Weight gain was higher in rats supplemented with glucomannan than in those without glucomannan supplements, but the difference is not significant. A lowering tendency in glucose levels was likewise observed. Furthermore, total cholesterol and HDL-cholesterol levels were lower and higher, respectively in diabetic rats receiving glucomannan. Although the triglyceride levels were similar in all rats, lipid peroxidase levels were significantly lower in rats with high-fiber diet.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1991 Sep
PMID:Effects of long-term high-fiber diet on macrovascular changes and lipid and glucose levels in STZ-induced diabetic SD rats. 165 79

The effect of diabetes mellitus induced by streptozotocin on the activities of peroxisomal oxidases and H2O2-metabolizing enzymes, and lipid peroxidation in various rat tissues were investigated. Peroxisomal acyl-CoA oxidase, D-amino acid oxidase and L-alpha-hydroxyacid oxidase were measured by a sensitive spectrophotometric method using dichlorofluorescein/peroxidase as the detector of H2O2. Acyl-CoA oxidase activity was increased most markedly in the heart of diabetic rats, less markedly in the liver, and tended to be increased in the kidneys. The activities of other peroxisomal oxidases were much lower than that of acyl-CoA oxidase in the liver and kidneys, and were undetectable in the heart. Catalase activity was decreased in the liver and kidneys of diabetics, and was increased in the heart. Glutathione peroxidase activity was increased more markedly in the kidneys of the diabetics, and less markedly in the heart than in the liver. Lipid peroxide level was higher in the kidneys of the diabetics than in the controls, unchanged in the heart, and was lower in the liver of the diabetics than in the controls. Thus, peroxisomal beta-oxidation and the H2O2 production coupled with that, were activated in various tissues of diabetic rats, presumably as a part of the overall increase in lipid oxidation. However, they did not appear to contribute to the enhanced oxidative stress induced by diabetes mellitus.
Diabetes Res Clin Pract 1991 Feb
PMID:Peroxisomal oxidases in various tissues of diabetic rats. 167 55

Soleus muscles of fed rats were fixed by vascular perfusion with paraformaldehyde; individual fibers were teased and immunostained with a polyclonal antibody against the COOH-terminal of GLUT4. The binding sites were visualized by a horseradish peroxidase-coupled secondary antibody and diaminobenzidine. The fibers were embedded in epoxy resin and studied by electron microscopy. Strong immunoreactivity was found in subsarcolemmal clusters of vesicles and cisternae, Golgilike structures, and triadic junctions. Clusters of vesicles between myofibrils were occasionally stained. The plasma membrane was unlabeled. However, the plasma membrane was labeled when the rats had been injected with insulin (40 U/kg body wt) 15 min before perfusion fixation. In non-insulin-injected rats, the plasma membrane might show spotty staining close to clusters of intensely labeled subsarcolemmal vesicles. This may have been due to diffusion but may also indicate that there are domains of GLUT4 in the plasma membrane of nonstimulated fibers or that the endogenous insulin activity to some extent had translocated GLUT4 from the intracellular pool into the plasma membrane. Coated vesicles that were also labeled were found adjacent to subsarcolemmal vesicles and cisternae; it is possible that coated vesicles play a role during insulin- or contraction-induced translocation of GLUT4 between subsarcolemmal pool and plasma membrane. It has been proposed that glucose uptake into skeletal muscle fibers takes place across the t-tubule membrane rather than across the plasma membrane. This would explain the presence of GLUT4 at triadic junctions. Alternatively, we suggest that GLUT4 in t-tubules represents a second intracellular pool.
Diabetes 1992 Feb
PMID:Subcellular localization of GLUT4 in nonstimulated and insulin-stimulated soleus muscle of rat. 173 12


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