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

Vitamin E has been shown to affect bone metabolism. In this study we determined the effects of palm vitamin E and alpha-tocopherol on bone metabolism. Sprague-Dawley female rats fed with normal rat chow were divided into 4 groups and supplemented with either palm vitamin E 30 mg/kg rat weight, palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight. One group was not supplemented. Half of these rats were ovariectomised before supplementation was given for 10 months. As expected, bone mineral density of the ovariectomised rats fed on normal rat chow diet was lower compared to the intact rats. However, these changes were not seen in the supplemented group of rats. Both intact and ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight had a lower bone calcium content in both femoral and vertebral bones whilst rats fed palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight were able to maintain bone calcium content. Alkaline phosphatase activity was elevated in ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight and alpha-tocopherol 30 mg/kg rat weight compared to the intact rats. Alpha-tocopherol also reduced the activity of tartrate-resistant acid phosphatase post-ovariectomy. These findings indicate that both palm vitamin E and alpha-tocopherol maintained bone mineral density in ovariectomised rats but caused conflicting effects on bone calcium content. Further study is needed in order to determine the mechanisms involved.
Exp Clin Endocrinol Diabetes 2000
PMID:Palm vitamin E is comparable to alpha-tocopherol in maintaining bone mineral density in ovariectomised female rats. 1096 63

We investigated the effects of diabetes mellitus and antioxidant treatment on the sensory and reflex function of cardiac chemosensory nerves in rats. Diabetes was induced by streptozotocin (STZ; 85 mg/kg ip). Subgroups of sham- and STZ-treated rats were chronically treated with an antioxidant, vitamin E (60 mg/kg per os daily, started 2 days before STZ). Animals were studied 6-8 wk after STZ injection. We measured renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MABP), and cardiac vagal and sympathetic afferent activities in response to stimulation of chemosensitive sensory nerves in the heart by epicardial application of capsaicin (Caps) and bradykinin (BK). In cardiac sympathetic-denervated rats, Caps and BK (1-10.0 microg) evoked a vagal afferent mediated reflex depression of RSNA and MABP, which was significantly blunted in STZ-treated rats (P < 0.05). In vagal-denervated rats, Caps and BK (1-10.0 microg) evoked a sympathetic afferent-mediated reflex elevation of RSNA and MABP, which also was significantly blunted in STZ-treated rats (P < 0.05). Chronic vitamin E treatment effectively prevented these cardiac chemoreflex defects in STZ-treated rats without altering resting blood glucose or hemodynamics. STZ-treated rats with insulin replacement did not exhibit impaired cardiac chemoreflexes. In afferent studies, Caps and BK (0.1 g-10.0 microg) increased cardiac vagal and sympathetic afferent nerve activity in a dose-dependent manner in sham-treated rats. These responses were significantly blunted in STZ-treated rats. Vitamin E prevented the impairment of afferent discharge to chemical stimulation in STZ rats. The following were concluded: STZ-induced, insulin-dependent diabetes in rats extensively impairs the sensory and reflex properties of cardiac chemosensitive nerve endings, and these disturbances can be prevented by chronic treatment with vitamin E. These results suggest that oxidative stress plays an important role in the neuropathy of this autonomic reflex in diabetes.
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PMID:Oxidative stress impairs cardiac chemoreflexes in diabetic rats. 1104 51

Increased oxidative stress is believed to be an important factor in the development of diabetic complications. In this study, the effect of diabetes on the susceptibility of synaptosomes to oxidative stress, induced by the oxidizing system ascorbate/Fe2+, on the activity of antioxidant enzymes and on the levels of glutathione and vitamin E was investigated. Synaptosomes were isolated from brain of 29-weeks-old Goto-Kakizaki (GK) rats, a model of non-insulin dependent diabetes mellitus and from normal Wistar rats. Synaptosomes isolated from GK rats displayed a lower susceptibility to lipid peroxidation, as assessed by quantifying thiobarbituric acid reactive substances (TBARS), than normal rats (5.33 +/- 0.79 and 7.58 +/- 0.7 nmol TBARS/mg protein, respectively). In the absence of oxidants, no significant differences were found between the levels of peroxidation in synaptosomes of diabetic or control rats. Superoxide dismutase (SOD), glutathione peroxidase and glutathione reductase activities were unaltered in the brain of diabetic rats. There were no statistically significant differences in fatty acid composition of total lipids and reduced glutathione levels in synaptosomes of diabetic and control rats. The decreased susceptibility to membrane lipid peroxidation of diabetic rats synaptosomes correlated with a 1.3-fold increase in synaptosomal vitamin E levels. Vitamin E levels in plasma were also higher in diabetic rats (21.32 micromol/l) as compared to normal rats (15.13 micromol/l). We conclude that the increased resistance to lipid peroxidation in GK rat brain synaptosomes may be due to the increased vitamin E content, suggesting that diabetic animals might develop enhanced defense systems against brain oxidative stress.
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PMID:Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress: role of vitamin E. 1112 43

The present study evaluated the effect of dietary vitamin E supplementation (1,000 mg/kg chow) on the alterations in vascular reactivity of streptozotocin-diabetic aorta of Wistar rats. After 12 weeks of treatment, thoracic aortic rings of rats were mounted in organ baths and contractile responses to phenylephrine and 5-hydroxytryptamine and relaxant responses to acetylcholine, calcium ionophore and sodium nitroprusside were assessed. Plasma vitamin E concentration as measured by HPLC was markedly decreased in diabetic rats and increased with dietary vitamin E supplementation. Induction of diabetes significantly impaired endothelium-dependent relaxations to acetylcholine and calcium ionophore in aortic rings, but did not change endothelium-independent relaxation to sodium nitroprusside. Vitamin E significantly improved the impaired endothelium-dependent relaxations, further it decreased the enhanced contractile response to phenylephrine and 5-hydroxytryptamine in diabetic rings. The mechanical denudation of endothelium or the chemical inhibition of endothelium-dependent relaxation with N(omega)-nitro-L-arginine methyl ester (100 micromol/l) significantly increased phenylephrine contractility in control rings and the rings of diabetic rats treated with vitamin E; such a difference was not observed in diabetic rats fed with normal diet. Liver and lung malondialdehyde concentrations, as an index of lipid peroxidation, were increased in diabetic rats and significantly decreased with vitamin E supplementation. It is concluded that dietary supplementation of vitamin E improved endothelial dysfunction in insulin-dependent model of uncontrolled diabetes, probably decreasing membranal lipid peroxidation.
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PMID:Effect of dietary vitamin E supplementation on vascular reactivity of thoracic aorta in streptozotocin-diabetic rats. 1115 Sep 23

Diabetes patients often show increased production of reactive oxidative species (ROS) together with vascular complications. The presence of these ROS may lead to increased DNA damage in peripheral blood lymphocytes that may be revealed by the comet assay. To test whether DNA is damaged in diabetes, peripheral blood samples were taken from 30 control individuals and 63 diabetic patients (15 insulin dependent (IDDM) and 48 non-insulin dependent (NIDDM)) and the alkaline comet assay was used to evaluate background levels of DNA damage. Significant differences were detected between control and diabetic patients in terms of frequencies of damaged cells. The extend of DNA migration was greater in NIDDM patients by comparison with IDDM patients which might indicate that IDDM patients are handling more oxidative damage on a regular basis. Smoker individuals had higher frequencies of cells with migration by comparison with the non-smokers in both groups. Also, clear differences between patients on placebo and on Vitamin E supplementation for 12 weeks were observed on the basis of the extend of DNA migration during single cell gel electrophoresis.
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PMID:Assessment of DNA strand breakage by comet assay in diabetic patients and the role of antioxidant supplementation. 1134 38

Previous studies hypothesised that vitamin E could protect against coronary heart disease and vascular complications in diabetes, but no studies have been performed regarding its eventual effects on fibrinolysis. Nevertheless, in Type 2 diabetes mellitus (T2DM) a profound reduction in the fibrinolytic activity has been demonstrated to be involved in vascular complications, probably due to plasminogen activator inhibitor type 1 (PAI-1) overproduction. On this basis we aimed to verify whether an antioxidant treatment with vitamin E is able to lower PAI-1 plasma levels in T2DM. Thirteen T2DM patients (9 males and 4 females; mean age+/-SD, 64.4+/-3.3 yr) were selected through strict admission criteria. These patients were treated with vitamin E (500 IU/die) for 10 weeks. Glyco-lipometabolic, oxidative and haemocoagulative parameters were evaluated at baseline and after 5, 10, 30 and 60 weeks. Vitamin E levels at different times were [median (interquartile range)] 6.1 (5.3-7.7), 8.5 (7.3-9.9), 9.7 (8.9-12.9), 5.6 (4.4-6.8), 5.7 (4.5-7.1) microg/ml, respectively. Significant differences were found for PAI-1 antigen (p=0.006), PAI-1 activity (p=0.028), apolipoprotein B (p=0.015) and antioxidant defence, evaluated as ferric reducing ability of plasma (FRAP) values (p=0.005). Particularly, decrements were detected for PAI-1 antigen between baseline and the 10th week (p<0.05), followed by an increase back to basal at the 30th week. Similar behaviour was found for PAI-1 activity. Regarding the antioxidant defence, FRAP values increased until the 30th week (p<0.05) with a decrease at the 60th week. These results demonstrate that vitamin E is able to lower PAI-1 levels in diabetic patients but this effect does not seem related to improvements of glycometabolic data or to the increase in FRAP values, suggesting that PAI-1 overproduction can be decreased by other effects of vitamin E on endothelial cells.
Diabetes Nutr Metab 2001 Apr
PMID:Vitamin E intake reduces plasminogen activator inhibitor type 1 in T2DM patients. 1138 76

We determined the effects of intraperitoneally administered vitamin C on the lipid peroxidation (as thiobarbituric acid-reactive substances, TBARS) and vitamin C and E levels and reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) activity in the plasma, red blood cells (RBC), liver, and muscle of rats in relation to oxidative damage associated with diabetes induced by streptozotocin (STZ). One group was used as control and a second as diabetic. A third group received 30 mg vitamin C i.p. every other day. On day 4 after the injection of vitamin C, animals in the second and third groups were made diabetic by i.p. injection of STZ and administered vitamin C for 21 consecutive days, and we determined TBARS, vitamin E, and GSH levels and GSH-Px activities in plasma, RBC, liver, and muscle samples. Vitamin E levels in the plasma and liver were significantly higher (P<0.05) in the control group than in the diabetic group. Also, TBARS levels in the plasma, RBC, liver, and muscle samples were significantly lower (P<0.05) in controls than in the diabetic group. The TBARS levels in the RBC, liver, and muscle samples of the vitamin C group were significantly lower (P<0.05, P<0.01, and P<0.001, respectively). However, GSH-Px and GSH activities in RBC, liver, and muscle and vitamin C levels in liver were not significantly different between control and diabetic groups. Vitamin E levels in plasma (P<0.05, P<0.01) and liver (P<0.001), vitamin C levels in liver (P<0.001), and GSH (P<0.01) and GSH-Px activities in RBC (P<0.05, P<0.01) were significantly higher in the vitamin C group than both the control and diabetic groups. These results indicate that vitamin C has significant protective effects on the blood, liver, and muscle of rats against oxidative damage in diabetes.
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PMID:Effects of intraperitoneally administered vitamin C on antioxidative defense mechanism in rats with diabetes induced by streptozotocin. 1142 72

Experimental and epidemiological evidence suggests that activation of the reninangiotensin-aldosterone system and oxidative modification of low density lipoprotein cholesterol both play important roles in atherosclerosis. A substudy of the HOPE (Heart Outcomes Prevention Evaluation) trial, the SECURE trial (Study to Evaluate Carotid Ultrasound changes in patients treated with Ramipril and vitamin E), evaluated the effects of long-term treatment with the angiotensin-converting enzyme (ACE) inhibitor, ramipril, and with vitamin E on atherosclerosis progression in high risk patients. A total of 732 patients were enrolled into the study. These patients were 55 years or older, had vascular disease or diabetes with at least one other cardiovascular risk factor, but did not have heart failure or low ejection fraction. Patients were randomly assigned according to a three-by-two factorial design to receive placebo, ramipril 2.5 mg/day or ramipril 10 mg/day and placebo or vitamin E 400 IU/day. Progression of atherosclerosis was evaluated by B-mode carotid ultrasonography. The primary outcome evaluated was the annualised progression slope of the mean maximum carotid intimal-medial thickness (IMT) across 12 pre-selected carotid arterial segments. The average follow-up was 4.5 years. The progression slope of the mean maximum IMT was 0.0217 +/- 0.04 mm/year in the placebo group, 0.018 +/- 0.44 mm/year in the ramipril 2.5 mg/day group and 0.0137 +/- 0.04 in the ramipril 10 mg/day group (P = 0.33 for the overall effect of ramipril and P = 0.028 for the comparison between patients receiving ramipril placebo and ramipril 10 mg/day). The reduction in atherosclerotic progression observed with ramipril remained significant after adjusting for systolic and diastolic blood pressure changes (P = 0.043) and after multivariate adjustment (P = 0.046). Administration of vitamin E 400 IU/day had no impact on atherosclerosis progression. The SECURE study is the first demonstration, in human subjects, of an effect of ACE inhibition on atherosclerotic progression. This benefit cannot be explained by the lowering of blood pressure alone. Vitamin E 400 IU/day had a neutral effect on the ultrasound measurements of atherosclerosis progression in the SECURE trial.
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PMID:Modifying the natural history of atherosclerosis: the SECURE trial. 1171 53

Poor diet and physical inactivity contribute to many chronic diseases in the United States each year. Diets low in saturated fatty acids and cholesterol and high in plant foods, i.e., fruits and vegetables, legumes and whole cereals, are protective. Physically active lifestyles are associated with lower risk of cardiovascular diseases, diabetes, obesity and some cancers. To access diet and physical activity levels in West Virginians, we conducted a study which was supported by the West Virginia Bureau for Public Health and the West Virginia University Prevention Research Center (CDC Cooperative Agreement). The purposes of this study were to estimate the proportion of the sample meeting recommendations for chronic disease prevention, and to examine if the individuals who were meeting the Surgeon General's physical activity recommendation for health are also consuming healthier diets. Our results showed that reducing saturated fatty acids and increasing consumption of folate, Vitamin E, calcium and fiber are of prime public health importance in West Virginia. Diet and activity levels were modestly related, suggesting that those who adopt a healthy diet also become more active and vice versa. Due to the cross-sectional nature of this data, it is unknown if single-strategy or dual interventions work best. Prospective studies are needed to determine optimal strategies.
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PMID:Dietary intakes and leisure-time physical activity in West Virginians. 1182 76

Oxidative stress is believed to be involved in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, and cataracts and to accelerate the aging process. The aim of this study was to elucidate the role of various dietary fats in the in vivo modulation of CCl(4) induced oxidative stress using rat as a model. Rats were raised on diets enriched with saturated (Beef Tallow), n-9 (Sunola oil), n-6 (Safflower oil) or n-3 (Flaxseed oil) fatty acids and exposed to elevated oxidative stress by administration of CCl(4.) Plasma concentration of 8-iso-PGF(2alpha), antioxidant micronutrients and antioxidant enzymes were measured to examine changes to oxidative stress subsequent to the administration of CCl(4). The fatty acid profiles of plasma and RBC membranes reflected the fats fed in the different diets. CCl(4) administration had no significant effect on fatty acid composition of plasma or RBC lipids. Plasma 8-iso-PGF(2alpha) concentrations were elevated by CCl(4) administration regardless of the dietary fat fed. Within the induced oxidative groups the 8-iso-PGF(2alpha) concentrations were highest in Safflower oil followed by Sunola oil, Tallow and finally Flaxseed oil. Induction of oxidative stress by CCl(4) administration was associated with a significant reduction in Vitamin A content reaching a significantly lower concentration (P <0.05) in the Tallow and Flaxseed oil groups. Vitamin E concentrations were significantly lower (p = 0.01) in the Safflower oil and the Flaxseed oil than in the Tallow diet group following CCl(4) administration. Superoxide Dismutase (SOD) and Glutathione Peroxidase (GSHPx) activities were not affected by dietary fat manipulation. The results of this study indicate that dietary fat can modulate lipid peroxidation and antioxidant defenses when exposed to a pro-oxidant challenge.
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PMID:Modulation of carbon tetrachloride-induced oxidative stress by dietary fat in rats(open star). 1183 24


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