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

The heart is one of the organs affected during the later stages of diabetes. Mitochondrial function has already been proposed to be affected during the course of diabetes. Nevertheless, little information is known concerning the impact of antioxidants in heart mitochondria of a milder model for diabetes, such as the Goto-Kakizaki (GK) rat, where mitochondrial function appears ameliorated. The objective of this work was to test if injections of Vitamin E and Coenzyme Q10, alone and in combination, were able to modify mitochondrial performance in the hearts of GK rats. Several aspects of mitochondrial function were measured, such as the respiratory control ratio and the electric potential, as well as the mitochondrial accumulation of Vitamin E and Coenzymes Q9 and Q10. We observed that only Vitamin E appeared to have a positive impact on the mitochondrial phosphorylation efficiency and on mitochondrial performance, namely on the ability to generate the electric transmembrane potential in the presence of supra-physiological calcium concentrations. Vitamin E administration also increased the mitochondrial concentration of Coenzyme Q10. None of the treatments was able to reverse the diabetic phenotype in GK rats. We conclude that in this model of mild hyperglycemia, administration of antioxidants may have a marginal positive impact on mitochondrial function.
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PMID:Vitamin E or coenzyme Q10 administration is not fully advantageous for heart mitochondrial function in diabetic goto kakizaki rats. 1612 Mar 65

Previously maternal and fetal alterations resembling human pre-eclampsia were induced in pregnant rats by injections of the angiogenesis inhibitor Suramin. These alterations were aggravated by maternal diabetes and partly rectified by vitamin E supplementation. In the present study we evaluated the morphology of placentae and kidneys in this model. Non-diabetic and streptozotocin-induced diabetic pregnant rats of two rat strains (U and H) were treated with Suramin or saline, and given standard or vitamin E-enriched food. On gestational day 20 one placenta and the left kidney of the mother were collected for morphological and stereological analysis. In the placental trophospongium Suramin treatment caused cysts, which were further enhanced by maternal diabetes. Vitamin E treatment had no effect on the vacuolization. In the placental labyrinth of the non-diabetic rats Suramin treatment restricted maternal placental blood volume and increased the interface between maternal and fetal circulation. These changes were reversed by vitamin E treatment. Diabetes increased slightly the interface between the circulations in both rat strains. Suramin treatment decreased the interface, and vitamin E further decreased the interface in the diabetic U rats, whereas neither treatment affected the maternal-fetal interface in the diabetic H rats. The kidneys of Suramin-treated and diabetic rats were heavier compared to controls. Suramin treatment and maternal diabetes damaged renal glomeruli to a similar extent. Vitamin E treatment diminished the Suramin- and diabetes-induced glomerular damage in U rats, but not in H rats. The average cell count per glomerulus was decreased by Suramin in the U rats. Vitamin E treatment did not affect cell number per glomerulus in any group. We conclude that Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction and pre-eclampsia, also from the histological perspective. The present work supports the notion that one important effect of untreated maternal diabetes may be impaired placentation, leading to oxidative stress, morphological damage, and compromised placental function.
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PMID:Suramin-restricted blood volume in the placenta of normal and diabetic rats is normalized by vitamin E treatment. 1692 Jan 89

Diabetes is associated with hyperglycemia, one of the most important causes of oxidative stress. Endogenous antioxidants are able to destroy the reactive species and create a balance between antioxidant and free radicals. In diabetes, the oxidative stress is increased due to the deficiency in the antioxidant defense. The intake of antioxidants, such as vitamin E, may reduce the oxidative stress associated with diabetes and hence help to restore the antioxidant defense system. The aim of this article was to investigate the effect of different doses of vitamin E on the biochemical parameters of normal and streptozotocin (STZ)-induced diabetic rats. Biochemical analysis was used to study the effect of this vitamin on the biochemical parameters of normal and diabetic rats. The plasma levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and gamma-glutamyl transferase (gamma-GT) were significantly increased after the onset of diabetes. In addition, STZ-induced diabetes also caused an increase in the level of blood urea nitrogen (BUN) and creatinine. Oral administration of vitamin E (0.2-0.4 mg daily) significantly (P < 0.05) decreased the plasma level of ALT, AST, and gamma-GT. In addition, there was a slight but not significant reduction in the plasma level of ALP. Parameters of kidney function, such as BUN and creatinine, were slightly reduced after the oral administration of vitamin E. The plasma level of electrolytes, such as calcium and sodium, also changed significantly (P < 0.00001) after the oral administration of vitamin E. Vitamin E ameliorates the metabolic and biochemical parameters of diabetic rats.
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PMID:Vitamin E ameliorates some biochemical parameters in normal and diabetic rats. 1715 19

Vitamin E has the ability to scavenge a wide spectrum of free radicals, including singlet oxygen, superoxide, and hydroxyl radicals. It has beneficial effects against several other disorders, such as atherosclerosis and ischemic heart disease, because it acts as a transcriptional regulator for gene expression via a transcription factor TAP. The beneficial effect of vitamin E on plasma insulin and glucagon levels was examined using radioimmunoassay technique. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin at a dose of 60 mg/kg body weight. Vitamin E was given at a dose of either 0.2 mg, 0.4 mg, or 0.8 mg per animal 10 days before and after the onset of diabetes. Vitamin E significantly (P < 0.05) increased plasma insulin levels in normal rats but failed to increase the plasma insulin level in diabetic rats. In contrast, vitamin E caused a significant (P < 0.05) reduction in plasma glucagon level in rats treated before and after the onset of diabetes. Vitamin E may ameliorate some diabetic complication via reduction in the level of circulating glucagon.
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PMID:Vitamin E decreases the hyperglucagonemia of diabetic rats. 1715 20

Oxidative stress and oxidative damage to tissues are common end points of chronic diseases such as atherosclerosis, diabetes, and rheumatoid arthritis. Oxidative stress in diabetes coexists with a reduction in the antioxidant status, which can further increase the deleterious effects of free radicals. The aim of the present study was to evaluate the possible protective effects of Murraya koenigii leaves extract against beta-cell damage and antioxidant defense systems of plasma and pancreas in streptozotocin induced diabetes in rats. The levels of glucose and glycosylated hemoglobin in blood and insulin, Vitamin C, Vitamin E, ceruloplasmin, reduced glutathione and TBARS were estimated in plasma of control and experimental groups of rats. To assess the changes in the cellular antioxidant defense system such as the level of reduced glutathione and activities of superoxide dismutase, catalase and glutathione peroxidase were assayed in pancreatic tissue homogenate. The levels of glucose, glycosylated hemoglobin, insulin, TBARS, enzymatic and non-enzymatic antioxidants were altered in diabetic rats. These alterations were reverted back to near control levels after the treatment of M. koenigii leaves extract. Transmission electron microscopic studies also revealed the protective nature of M. koenigii leaves on pancreatic beta-cells. These findings suggest that M. koenigii treatment exerts a therapeutic protective nature in diabetes by decreasing oxidative stress and pancreatic beta-cell damage. The antioxidant effect of the M. koenigii extract was compared with glibenclamide, a well-known hypoglycemic drug.
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PMID:Beneficial effects of Murraya koenigii leaves on antioxidant defense system and ultra structural changes of pancreatic beta-cells in experimental diabetes in rats. 1718 70

Diabetes is clearly associated with accelerated atherosclerosis development, but molecular mechanisms involved in diabetes-induced atherosclerosis remain to be clarified. The aim of this study was to identify cellular mechanisms involved in diabetes-induced macrophage foam cell formation, the hallmark of early atherogenesis. Mouse peritoneal macrophages (MPMs) isolated from Balb-C streptozotocin-induced diabetic mice, exhibited significantly higher total peroxides, lipid peroxides and paraoxonase 2 (PON2) activity by 290%, 61% and 55%, respectively, compared to non-diabetic mice. In vitro studies revealed that glucose-induced oxidative stress was obtained by D-glucose, but not by L-glucose and it involved activation of the NADPH oxidase complex, and up-regulation of the macrophage PON2. Next, MPMs isolated from Balb-C diabetic mice, compared to control Balb-C mice, demonstrated increased cholesterol content by 4.2-fold associated with increased cholesterol biosynthesis and increased uptake of oxidized LDL (Ox-LDL) by 5.9-fold and 31%, respectively. These effects on cellular cholesterol metabolism were associated with up-regulation of the scavenger receptors for Ox-LDL (CD-36 and SR-A), and of HMG-CoA reductase (cholesterol biosynthesis rate limiting enzyme). Finally, using pravastatin (inhibitor of HMG-CoA reductase) and the antioxidant Vitamin E, we have shown that D-glucose-induced macrophage oxidative stress is secondary to its stimulatory effect on macrophage cholesterol biosynthesis. In conclusion, macrophages from diabetic mice demonstrate increased oxidative stress associated with activation of NADPH oxidase and up-regulation of cellular PON2, as well as increased macrophages cholesterol uptake and biosynthesis (increased expression of CD-36 and HMG-CoA reductase). The above mechanisms in diabetic mice could be the result of the effect of high D-glucose on macrophages.
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PMID:Macrophage NADPH oxidase activation, impaired cholesterol fluxes, and increased cholesterol biosynthesis in diabetic mice: a stimulatory role for D-glucose. 1725 48

The present study was designed to evaluate the effect of Vitamin E (Vit. E) on diabetes-induced changes in small intestine, lipid peroxidation and plasma antioxidant capacity in rats. Twenty-four rats were divided into three groups (n=8), namely control, non-treated diabetic (NTD) and Vit. E-treated diabetic (VETD) groups. The VETD group received 300 mg of Vit. E daily in drinking water. After 6 weeks, the length and weight of small intestine, villus height, crypt depth and muscular layer thickness showed a significant increase in the NTD group compared to the control group. In the VETD group, these parameters did not show any significant difference compared to the control group. The level of malondialdehyde (MDA) in the red blood cells showed a significant increase in the NTD group, but not in the VETD group, compared to the control group. The plasma antioxidant capacity showed a significant increase in VETD compared to the NTD group. These findings indicate that Vit. E significantly improved small intestinal changes in diabetic rats and that these effects could be mediated at least in part by enhanced plasma antioxidant capacity and reduced lipid peroxidation.
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PMID:Effect of vitamin E on diabetes-induced changes in small intestine and plasma antioxidant capacity in rat. 1745 Nov 58

In studies of vitamin E effectiveness in diabetes, there are still controversies surrounding negative observational and positive experimental results. However, there is no controversy that antioxidant vitamin E is regenerated from its pro-oxidant tocopheroxyl radical by a network of interacting co-antioxidants. The network of interacting co-antioxidants has only been studied individually. The hypothesis we propose is that a vitamin E regeneration system (VERS) model based on the complex interactions of the co-antioxidants provides a rationale for vitamin E supplementation as a therapeutic adjunct in diabetes. Furthermore, the factors considered prior to the use of Vitamin E as a supplement in diabetes research and therapy, the effectiveness of vitamin E supplementation and the limitations have been identified in the literature. There is no single study of vitamin E supplementation or efficacy that has determined vitamin E levels in combination with all of the co-antioxidants that interact to regenerate oxidised vitamin E. Therefore, there is a lack of good evidence for or against vitamin E being unilaterally depleted in the antioxidant network. There is also lack of rationale for choice of co-antioxidant supplementation. In essence, the normal conditions for effective antioxidant activity of vitamin E supplementation have yet to be fully explored. We propose a coherent model of VERS, and recommend that VERS status needs to be assessed, as part of evidence-based clinical practice to determine whether vitamin E should be recommended for the diabetic patient. We also propose an algorithm, based on the antioxidant activity and confounding factors, to guide the formulation of a credible hypothesis for clinical trials in assessing the function of vitamin E and treatment outcomes. The proposed model hinges on pertinent questions that have to be addressed to avoid organising a clinical trial that has been identified as biased.
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PMID:The 'vitamin E regeneration system' (VERS) and an algorithm to justify antioxidant supplementation in diabetes--a hypothesis. 1795 21

Membranes formed of thermodynamically stable cubic phase lyotropic liquid crystals (LLCs) could replace the presently used polymeric membranes, applied to reduce the flux of glucose in semicontinuous, subcutaneously implanted, user-replaced, miniature, amperometric glucose sensors, assisting in the management of diabetes. LLC-forming amphiphilic compounds set and toughen spontaneously after mixing with water, without undergoing chemical change. When applied by doctor-blading, they form membranes having three-dimensionally interconnected water channels of uniform diameter, with reproducible glucose transport-characteristics. We find that the best studied cubic phase LLCs, which are formed of monoolein and water, are not useful in their intended application because they are hydrolyzed by serum lipases. Those formed of phytantriol, a liquid at ambient temperature, and water, are not hydrolyzed but change their shape and size in a dehydration and rehydration cycle. Because glucose sensors are sterilized and stored in a sealed package in a dry atmosphere, drying and rehydration must not change the transport characteristics. A third, novel, LLC-forming, amphiphile 1-O-beta-(3,7,11,15-tetramethylhexadecyl)-d-ribopyranoside, I, was synthesized, and its phase diagram was tailored by adding Vitamin E acetate, to form a cubic phase. The phase was stable through the 20 degrees C-90 degrees C temperature range in excess of water and had the desired glucose-transport characteristics. A preferred LLC, II, was formed of water and I containing 7 wt % of Vitamin E acetate. When II was applied to a wired glucose oxidase bioelectrocatalyst, sensors of reproducible glucose-sensitivity were formed. At a 0.1 mm thickness of II, the membrane reduced the glucose flux 5-fold and increased the 90% response-time by less than 2 min. The membrane was mechanically rugged, withstanding the approximately 1 N m(-2) maximal shear stress at 5 mm diameter electrodes rotating at 4000 rpm. The activation energy for glucose permeation through II was reduced to 15.6 kJ/mol, making the sensors's current less temperature-dependent than that of the polymeric-membrane overcoated implantable glucose sensors.
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PMID:Liquid crystal membranes for serum-compatible diabetes management-assisting subcutaneously implanted amperometric glucose sensors. 1824 85

Streptozotocin destroys the beta-cells of pancreas by generation of reactive oxygen species and vitamin E has documented antioxidant properties. To evaluate the preventive effect of vitamin E on induction of diabetes by streptozotocin and effect of oral vitamin E consumption on carbohydrate and lipid metabolism, forty male Wistar rats divided randomly to control, E1, E2 and E3 groups. The diet of E1, E2 and E3 groups were supplemented with 1, 2 and 4 g kg(-1) of vitamin E, respectively. Four days later all rats were made diabetic by IP injection of 45 mg kg-' streptozotocin and blood glucose was measured 72 h later to determine the severity of blood glucose elevation. Glycosylated hemoglobin, triglyceride, total cholesterol and HDL-c were measured and LDL-c and VIDL-c calculated in plasma of 6 diabetic rats with glucose more than 200 mg dL(-1) in each groups 21 days after streptozotocin injection. Vitamin E had no effect on diabetes induction by streptozotocin, but elevation of glycosylated Hb and reduction of LDL-c in group E3 were significant. Vitamin E also increased HDL-c although it was not statistically significant. We suggest that oral vitamin E consumption may have some beneficial effect on the correction of lipid metabolism disorders of diabetes, although it may worsen carbohydrate metabolism in mild diabetes.
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PMID:The effects of oral vitamin E on induction and consequence of experimental diabetes mellitus in rats. 1881 39


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