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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The subcellular and macromolecular distribution of 75Se-selenite was determined in murine mammary epithelial cell lines which demonstrated marked differences in their growth response to 5 microM selenite. MOD cells responded sooner to the inhibitory effects of selenite than COMMA-D cells. The MOD cells also incorporated a slightly higher percentage of 75Se-selenite into proteins and attained a higher ratio of selenoprotein to selenonucleic acids than did COMMA-D cells. Most selenium and selenoproteins were located in the cytoplasm as revealed by autoradiography and subcellular fractionations. These data suggest that a cytoplasmic selenoprotein may be an intermediate for selenite's nontoxic growth inhibitory effects.
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PMID:Selenium distribution in mammary epithelial cells reveals its possible mechanism of inhibition of cell growth. 245 95

Resolution of selenium-containing proteins synthesized by mouse mammary gland cells was achieved using the technique of two-dimensional gel electrophoresis. Radioactive selenium as H2[75Se]O3 was incorporated into relatively few proteins within mammary gland cells maintained in vitro and cells of mammary gland tissue in vivo. The pattern of selenoproteins obtained was identical qualitatively between a nontumorigenic differentiated cell line, COMMA-D, and a tumorigenic cell line, MOD. Eleven selenoproteins ranging in molecular weight from 12,000-78,000 were detected and a total of 25 spots were visible indicating charge heterogeneity of some of the proteins. A major selenoprotein (Mr 26,000) migrated identically with the subunit form of glutathione peroxidase, a well-characterized protein containing four selenocysteine residues. Other major selenoproteins had molecular weights of 58,000, 22,000, 18,000, and 14,000. Analysis of the total cellular protein extract and of each of the five major proteins indicated that selenium was incorporated as selenocysteine in the proteins. Incorporation of selenium as selenomethionine into cellular proteins was detected only when selenomethionine was provided in the culture medium. Cleavage of 75Se-labeled proteins with N-chlorosuccinimide produced polypeptides of different molecular weights indicating that the Mr 58,000, 26,000, and 22,000 selenoproteins were dissimilar in the amino acid sequences containing the selenoamino acid. The pattern of selenoproteins of mammary gland cells in vivo was similar to that obtained for cells in culture and most other tissues in vivo. These results provide evidence for the presence of multiple selenium-containing proteins in mammary epithelial cells. The possible significance of these proteins in selenium-mediated inhibition of cell growth awaits future clarification.
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PMID:Distribution of selenoproteins in mouse mammary epithelial cells in vitro and in vivo. 294 39

Triphenylselenonium chloride, a novel synthetic organic selenium compound in which selenium is bonded to three unsubstituted benzene rings, possesses significant chemopreventive activity against chemically-induced mammary carcinogenesis. The effects of triphenylselenonium chloride on a mammary tumor cell line (MOD) were compared to selenite, a reference compound in selenium chemoprevention research. It was observed that triphenylselenonium chloride treatment exerted a cytostatic effect in the absence of membrane damage or DNA strand breaks. The observed cytostasis was associated with a selenium concentration-dependent inhibition of cell proliferation, measured by [3H]thymidine incorporation into DNA, and delayed cell cycle progression. In contrast, selenite treatment rapidly induced DNA damage and cell death. These marked differences were observed across the same levels of cellular selenium. In addition, triphenylselenonium chloride treatment increased glucose consumption and lactate production, indicating an effect of the compound on cellular energy metabolism. Collectively these observations demonstrate that the toxic activities associated with selenite treatment do not occur when cells are treated with triphenylselenonium chloride. This compound represents a new type of selenium compound that exerts significant cellular effects through mechanisms distinct from those induced by selenite.
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PMID:Cellular and metabolic effects of triphenylselenonium chloride in a mammary cell culture model. 769 7

The effects of two types of selenium compounds on the expression levels of growth arrest and DNA damage-inducible (gadd) genes and on selected cell death genes were examined in mouse mammary MOD cells to test the hypothesis that the diversity of selenium-induced cellular responses to these compounds could be distinguished by unique gene expression patterns. Whereas the expression patterns of known cell death-related genes (bcl-2 and bax) were not informative with respect to the cellular response patterns upon exposure to selenium compounds, time-dependent and selenium species-specific induction patterns were observed for gadd34, gadd45 and gadd153 genes. It was also observed that the MOD cells expressed a truncated p53 transcript but no detectable immunoreactive P53 protein, indicating a null p53 phenotype. The fact that selenium compounds induced growth arrest and death of these cells and that these compounds induced specific patterns of expression of gadd genes indicates that these genes may mediate some selenium-induced cellular responses. The findings further imply that selenium compounds may be effective chemopreventive agents for human breast carcinogenesis, in which p53 mutations are frequent.
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PMID:Differential induction of growth arrest inducible genes by selenium compounds. 917 4

Significantly more information about trace element status can be obtained by investigating concentrations in blood cells instead of only evaluating the concentrations in plasma. This can be explained by the fact that essential trace elements such as zinc, copper, chromium and selenium take part in a variety of enzymatic processes on a molecular cellular level. Ignoring these important biochemical roles, trace element concentrations determined in whole blood or plasma very often lead to conclusions contrary to the actual intracellular concentration. Especially in metabolic diseases like diabetes mellitus, conclusions drawn from trace element concentrations in blood cells usually offer more valuable clinical information about the metabolic state than trace element concentrations in plasma or whole blood. In the present investigation copper and zinc concentrations were increased in all blood fractions of diabetic patients (IDDM). In insulin-dependent diabetic children significantly higher values of zinc in erythrocytes were also found, and they were higher in patients with poor metabolic control (HbA1c>9%). When different blood fractions in diabetic patients (NIDDM) were compared with a control group, chromium was significantly increased in plasma and polymorphonuclear cells. Patients with IDDM had pronounced decreased selenium concentrations in erythrocytes as compared to controls.
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PMID:Trace elements in diabetes mellitus. Peculiarities and clinical validity of determinations in blood cells. 1083 30

This study aimed to compare the trace element status of patients with type 2 diabetes (n = 53) with those of nondiabetic healthy controls (n = 50). The concentrations of seven trace elements were determined in the whole blood, blood plasma, erythrocytes, and lymphocytes of the study subjects. Vanadium and iron levels in lymphocytes were significantly higher in diabetic patients as compared to controls (p < 0.05 for iron and p < 0.01 for vanadium). In contrast, lower manganese (p < 0.01) and selenium (p < 0.01) concentrations were detected in lymphocytes derived from patients with type 2 diabetes versus healthy subjects. Furthermore, significantly lower chromium levels (p < 0.05) were found in the plasma of diabetic individuals as compared to controls. Trace element concentrations were not dependent on the degree of glucose control as determined by correlation analysis between HBA1c versus metal levels in the four blood fractions. In summary, this study primarily demonstrated that trace element levels in lymphocytes of patients with type 2 diabetes could deviate significantly from controls, whereas, in general, no considerable differences could be found when comparing the other fractions between both patient groups. Therefore, it seems reasonable to analyze metal levels in leukocytes to determine trace element status in patients with type 2 diabetes and perhaps in other diseases.
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PMID:Concentrations of seven trace elements in different hematological matrices in patients with type 2 diabetes as compared to healthy controls. 1135 46

Imbalances between mineral intakes and recommended amounts have been observed in different groups of elderly subjects. Nevertheless, assessment of the status of magnesium and trace elements in the elderly is difficult, even for iron because infection and inflammation increases ferritin. Mineral bioavailability may change due to ageing. Therefore, formulation of mineral recommendations is complex and individual recommendations are sometimes necessary. A number of surveys show magnesium, zinc, selenium and chromium intakes by old persons to be lower than the corresponding reference nutrient intakes. Contrarily, intakes of iron are generally adequate or higher than recommended, and it has been suggested that increased storage of iron in the elderly may be related with the development of age-related diseases through the increase in oxidative stress. Low iron status together with iron excess may be common in an elderly population. The same applies for zinc. Magnesium and selenium deficiencies among the elderly are also well documented, especially among the institutionalised and people with pathologies. Chromium deficiency is associated with type II diabetes mellitus. Recommended iron intake is lower for elderly women compared to young, because menstruation ceases after menopause, but in old men, it is similar to that of young men. Dietary Reference Values for the rest of the elements are similar to those of adults, although several suggestions have been made about the quantities. This review examines various aspects of the changes in mineral bioavailability due to ageing, of data published on mineral intakes and status, and finally the dietary recommendations for this vulnerable population group.
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PMID:Magnesium and trace elements in the elderly: intake, status and recommendations. 1216 71

It was investigated the influence of a diet supplemented with selenium on the clinicometabolic parameters and the activity of lipid peroxidation in 43 patients with Type 2 diabetes mellitus. It was indicated that under the influence of dietotherapy besides the decrease of glucose levels in capillary and venous blood, improvement of parameters of lipid metabolism, a reduction of malondialdehyde level and tendency to increase of glutathione peroxidase activity were observed. The results of investigations testify about sufficiently expressed efficacy of a diet supplemented with selenium in correction of oxidative stress and clinicometabolic parameters in this contingent of patients.
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PMID:[Effect of selenium enriched diet on lipid peroxidation in patients with diabetes mellitus type 2]. 1266 92

Nevi, or moles, are localized nevocytic tumors. The American Cancer Society's "ABCD" rules are useful for differentiating a benign nevus from malignant melanoma. While acanthosis nigricans may signal an underlying malignancy (e.g., gastrointestinal tumor), it more often is associated with insulin resistance (type 2 diabetes, polycystic ovary syndrome) or obesity. Melasma is a facial hyperpigmentation resulting from the stimulation of melanocytes by endogenous or exogenous estrogen. Treatments for melasma include bleaching agents, laser therapy, and a new medication that combines hydroquinone, tretinoin, and fluocinolone acetonide. Lesions that develop on the shins of patients with diabetic dermopathy often resolve spontaneously; no treatment is effective or recommended. Tinea versicolor responds to treatment with selenium sulfide shampoo and topical or oral antifungal agents. Postinflammatory hyperpigmentation or hypopigmentation can occur in persons of any age after trauma, skin irritation, or dermatoses.
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PMID:Common hyperpigmentation disorders in adults: Part II. Melanoma, seborrheic keratoses, acanthosis nigricans, melasma, diabetic dermopathy, tinea versicolor, and postinflammatory hyperpigmentation. 1465 5

Insulin resistance, a hallmark of type 2 diabetes, is associated with oxidative stress. However, the role of reactive oxygen species or specific antioxidant enzymes in its development has not been tested under physiological conditions. The objective of our study was to investigate the impact of overexpression of glutathione peroxidase 1 (GPX1), an intracellular selenoprotein that reduces hydrogen peroxide (H(2)O(2)) in vivo, on glucose metabolism and insulin function. The GPX1-overexpressing (OE) and WT male mice (n = 80) were fed a selenium-adequate diet (0.4 mg/kg) from 8 to 24 weeks of age. Compared with the WT, the OE mice developed (P < 0.05) hyperglycemia (117 vs. 149 mg/dl), hyperinsulinemia (419 vs. 1,350 pg/ml), and elevated plasma leptin (5 vs. 16 ng/ml) at 24 weeks of age. Meanwhile, these mice were heavier (37 vs. 27 g, P < 0.001) and fatter (37% vs. 17% fat, P < 0.01) than the WT mice. At 30-60 min after an insulin challenge, the OE mice had 25% less (P < 0.05) of a decrease in blood glucose than the WT mice. Their insulin resistance was associated with a 30-70% reduction (P < 0.05) in the insulin-stimulated phosphorylations of insulin receptor (beta-subunit) in liver and Akt (Ser(473) and Thr(308)) in liver and soleus muscle. Here we report the development of insulin resistance in mammals with elevated expression of an antioxidant enzyme and suggest that increased GPX1 activity may interfere with insulin function by overquenching intracellular reactive oxygen species required for insulin sensitizing.
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PMID:Development of insulin resistance and obesity in mice overexpressing cellular glutathione peroxidase. 1518 68


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