• Journal of the East Asian Society of Dietary Life
• /
• v.9 no.4
• /
• pp.427-434
• /
• 1999

This study was conducted to investigate the effects of vitamin I supplementation on renal function in high fat diet and adriamycin (ADR) induced experimental nephrotic syndrome in model rats. The effects of vitamin E supplementation on renal function in high fat diet and ADR treated rats were as follows. Kidney weight was decreased by vitamin E supplementation. Serum total protein was increased by the excess supplementation. Blood urea nitrogen(BUN) was decreased by the high supplementation. However, serum albumin and creatinine showed no significant differences between groups. Urinary volume tended to increase by vitamin I supplementation. Urinary urea-N tended by vitamin I supplementation. Particularly glomerular filtration rate(GFR) was significantly decreased by vitamin E supplementation. These results suggested that vitamin E supplementation could alleviate the adverse effects caused in renal function by highfatdiet and ADR treatments.

• Journal of Nutrition and Health
• /
• v.33 no.2
• /
• pp.141-146
• /
• 2000

This study was conducted to investigate the effects of vitamin E supplementation renal lipid peroxidation in high fat diet and adriamycin (ADR) induced experimental nephrotic syndrome model rats. Treated rats were injected intraperitoneally with ADR (2mg/kgBW/wk) once a week for four weeks. control rats were injected with saline solution instead of ADR. The rats in each group were fed experimental diets of three levels of vitamin E for 10 weeks: Normal (501U/kg diet), high (5,000IU/kg diet), excess (7,500IU/kg diet). The high fat diet and ADR treatment was performed to induce the decrease of kidney functions. Serum total cholesterol was significantly decreased by the excess supplementation. But there was no effect of vitamin E supplementation on serum total lipid and triglyceride. Thiobarbituric acid reacting substances(TBARS) was significantly decreased at high and excess supplementation. Glutathione reductase (GR), glutathione peroxidase ({TEX}$GP_{x}${/TEX}) and catalase activities (CAT) were measured as antioxidative enzymes. The renalglutathione reductase (GR) and catalase activities (CAT) were inclined to elevate by vitamin E supplementation. Thus the vitamin E supplementation was found to have an antioxicant effect. These results suggested that vitamin E supplementation could alleviate the changes in renal lipid peroxidation.

• Journal of Nutrition and Health
• /
• v.31 no.8
• /
• pp.1226-1234
• /
• 1998

The aim of the study was to determine whether vitamin E supplementation in three experimental model rats with impaired glucse tolerance could change serum insulin concentration and lipid distribution. The three groups were adult(AS) and neonatal (NS) streptozotocin-induced groups, and a high sucrose diet(HS) group. Each group was divided into control and vitamin E supplementatino groups at the age of 9 weeks. The level of vitamin E supplementation was 5g/kg diet. Blood and organ samples were taken at 5 and 10 weeks and were examined for changes in the level of serum insulin, glucose, lipids, liver lipids, and oxidative status. Vitamin E supplementation significantly reduced serum insulin in the HS group and caused the significant beneficial changes in serum lipids and triglycerides in As grouop at 10 weeks . In all groups, serum vitamin E was increased and malondialdehyde(MDA) in serumand liver were decreased significantly by vitamin E supplementation. The results suggest that vitamin E supplementation improves lipid distribution in adult streptozotocin-induced rats and serum insulin concentration in high sucrose diet-induced rats. Vitamin E might prevent on reduce oxidative injury in all experimental model rats with impaired glucose tolerance.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.27 no.1
• /
• pp.149-156
• /
• 1998

The purpose of this study was to investigate the effects of vitamin E supplementation on the activities of antioxidative enzymes in liver of KK mice of various ages and various duration of diabetes. Diabetes was induced by feeding high fat diet containing 20% corn oil(wt/wt). Weaned KK mice were fed high fat diet containing 51 IU or 2080 IU vitamin E per kg diet. Animals were sacrificed at 4, 6, and 9 months of age. In nondiabetic group, we found the decrease of antionxidative enzyme activities with aging. In diabetic group, antioxidative enzyme activities were decreased, and the change of hepatic vitamin E was related to glutathione peroxidase activity (r=0.71, p<0.001). Treatment with vitamin E did not modify the level of fasting blood glucose. However, it was observered that glutathione reductase and glutathione peroxidase activities as well as hepatic glutathione levels were increased by vitamie E supplementation, whereas catalase activity did not changed. The present result suggest that high vitamin E supplementation protects against lipid peroxidative damage in diabetic KK mice.

• Journal of Nutrition and Health
• /
• v.31 no.2
• /
• pp.153-158
• /
• 1998

The purpose of this study was to investigate the effect of vitamin E supplementation on the lipid peroxidation and activities of antioxidative enzymes in the pancreas of diabetic KK mice. KK mice were fed high ft diet containing 20% corn oil(wt/wt), and sacrificed at 2 months of diabetes. A hish vitamin E diet consisted of the high fat diet supplemented with an excessive amount of 이-$\alpha$-tocopheryl acetate (2080IU/kg diet). The incidence of diabetes mellitus was 61% when mice were fed the high fat diet, but was 44% when mice were fed the high vitamin E diet, Vitamin E supplementation fhus seems to have the effect of decreasing of decreasing the onset of diaetes. In the diabetic group, we found increases of MDA (malondialdehyde) and antioxidative enzyme activities. Treatment with vitamin E did not modify the level of fasting blood glucose. However, MDA and antiosicative enzyme activities in diabetic mice were decreased by the high vitamin E diet. Increased levels of lipid peroxidation products suggests the occurrence of oxidative damage in the pancreas of diabetic mice. The increased level of antiosicative enzyme activities could be due to an adaptive response to conditions of increased peroxidative stress. Significant normalization on catalase activity was noted in vitamin E supplemented animals.

• Journal of Nutrition and Health
• /
• v.30 no.10
• /
• pp.1153-1159
• /
• 1997

We investigated the effects of vitamin E supplementation on lipid peroxidation and on the activities of antioxidative enzymes in kidney of KK mice of various age and duration of diabetes. Weaned KK mice were fed high fat a diet containing 20% corn oil(wt/wt), and were sacrificed at 4, 6, and 9 months of age. The high vitamin E diet consisted of the high fat diet supplemented with an excessive amount of dl-$\alpha$-tocopheryl acetate (2080 IU/kg diet) . In the diabetic groups, we found an increase in lipofuscin and decrease in antioxidative enzyme activities with aging. Treatment with vitamin E did not modify the level of fasting blood glucose. However, a significant decrease in lipofuscin and increase in antioxidative enzyme acitvities were observed in diabetic mice.

• Nutritional Sciences
• /
• v.1 no.1
• /
• pp.22-28
• /
• 1998

Plasma concentrations of Vitamins E and A were measured in 15 non-insulin dependent Korean female subjects and 15 age-matched normal subjects using reversed-phase high-performance liquid chromatography. No differences were found in plasma Vitamin E concentrations between the 2 groups. Plasma Vitamin A concentrations were higher in subjects with non-insulin dependent diabetes melitus (NIDDM). The effects were evaluated of 4 weeks of daily supplementation of 400 mg Vitamin E on plasma levels of these two vitamins. In addition, the effects were observed for Vitamin E supplementation on oxidative stress and immune-related compound productions in non-insulin dependent diabetic patients and control subjects. After treatment with Vitamin E, plasma Vitamin E concentrations were significantly elevated in both groups. Basal plasma thiobarbituric acid reactive substances (TBABS) were identical, and a decreased level of TBARS caused by Vitamin E was observed only in the diabetic group (0.02739$\pm$0.0024 versus 0.01814$\pm$0.0008 nmols malondialdehyde equivalents/dl plasma ; p<0.05). The basal and after-treatment levels of immunoglobulins A, G, M were identical in control and diabetic groups, indicating that Vitamin E did not appear to alter gross humoral responses in this study. However, elevation of Complement 3 ($C_3$) was noticed due to Vitamin E supplementation, revealing a possible effect of vitamin E on one aspect of humoral immunity, Furthermore, an increase in prostaglandin E_2 ($PGE_2$) levels in diabetic patients was normalized by Vitamin E supplementation. This suggests indirectly that the depressed cell-mediated response due to elevated $PGE_2$ could be normalized. For the definitive antioxidant intake recommendations for prevention and treatment of adverse effects of non-insulin dependent diabetes, evidence from intervention trials like this study should be collected. The present data suggests that Vitamin E may oxen some protective effects against oxidative damage and might have beneficial effects of partial immune-stimulation.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.26 no.5
• /
• pp.914-919
• /
• 1997

We investigated the effects of vitamin E supplementation on the protein glycosylation in vivo. Weaned KK-mice were fed high fat diet containing 20% corn oil(wt/wt), and sacrificed at 4, 6, and 0 months of age. High vitamin E diet was the high fat diet supplemented with an excess amount of 이-$\alpha$-tocopheryl acetate(2080IU/kg diet). We measured $HbA_{1C}$ as a glycosylation early product, and collagen-linked fluorescence (CLF) of skin as a glycosylation and product. We found that diabetic group had increased levels of $HbA_{1C}$ within 2 months after onset of diabetes and during the experiments. The skin CLF increased dramatically 5 months after onset of diabetics. Treatment with vitamin E did not modify the level of blood glucose. However, we observed a significant lowering in CLF and $HbA_{1C}$ in diabetic mice.

• Journal of Nutrition and Health
• /
• v.28 no.10
• /
• pp.967-975
• /
• 1995

To investigate effects of dietary fish oil and vitamin E level on the tissue levels of vitamin E and vitamin A and to see which tissue is sensitive to lipid peroxidizability, male Sprague-Dawley rats were fed experimental diets composed of either menhaden oil or soybean oil nad either low(equivalent to 17 mg $\alpha$-tocopherol) or high (equivalent to 140mg $\alpha$-tocopherol) vitamin E level for 4 weeks. Palsma TBARS per mg lipid was significantly elevated in rats fed fish oil with low vitamin E level compared to soybean oil-fed rats. TBARS levels of liver, heart, kidney and liver microsomes were also increased by feeding fish oil with low vitamin E level. Plasma TBARS level was significantly correlated with TBARS levels of liver, heart, kidney and liver microsome. Plasma vitamin E level of groups with vitamin E supplementation was elevated significantly as compared to the those without vitamin E supplementation, whereas vitamin E levels of liver, heart and kidney were not changed significantly. Plasma TBARS was negatively correlated with plasma vitamin E(r=0.5763, P<0.001) and A(r=-0.4523, P<0.01) and seems to be a good indicator of in vivo lipid peroxidative stress.

• Journal of Nutrition and Health
• /
• v.32 no.6
• /
• pp.644-653
• /
• 1999

Background : Excessive intakes of $\omega$6 polyunsaturated fatty acid (PUFA) can increase oxidative stress, which may increase insulin resistance and could be the cause of metabolic syndrome X such as diabetes mellitus. One of the ways to reduce oxidative stress is the consumption of antioxidants such as vitamin E. It is controversial that vitamin E intakes may alleviate insulin resistance. The purpose of the study was whether high vitamin E intake may influence whole body glucose disposal rate(GDR), glycogen deposites, triglyceride content, lipid peroxide levels and antioxidant enzyme activities in Sprague Dawley rats fed high $\omega$6 PUFA diest. Methods : Sprague Dawley rats were divided into three groups. The control group consumed chow diet. High and low vitamin E groups consumed 40% PUFA of total energy intakes. One kilogram of diet mixture contained 300IU of $\alpha$-tocopherol in high vitamin E group, while it had 30 IU in low vitamin E group. Diets were given for 8 weeks. After 7 were of diet consumption, indwelling catheters were inserted in carotid artery and jugular vein of all rats so that GDR could be measured in awake and unstressed state. Results : Daily PUFA intakes were lower in the control group than others. Daily vitamin E intake of high vitamin E group was about ten times higher than those of low vitamin E group and the control group(p<0.0001). $\alpha$-tocopherol content in lier was highest in the high vitamin E group. GDR of the control group was 24% higher than others, and vitamin E intakes did not affect GDR. Glycogen deposit of liver in the control group was significantly higher than others, and it was not altered by vitamin E supplementation. Muscle glycogne content showed a similar tendency as liver glycogen in different diet groups. Triglyceride deposit in muscle was not different among groups. Lipid peroxide content of liver in the high vitamin E group was lower than the low of glutathione peroxidase were lowered in low vitamin E group than others, however, those of superoxide dismutase and catalase were not different. Conclusions : High vitamin E intakes can decrease oxidative stress in rats fed high (())-6 PUFA diet, but they cannot alleviate insulin resistance. Thus, increased oxidative stress through high (())-6 PUFA diet may be minimal for influencing insulin resistance.