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

We tested the hypothesis that free radicals play a role in the selective destruction of pancreatic beta-cells in BB/Wor rats. Diabetes-prone BB rats of both sexes and 40 days of age were divided into three groups. The control group was fed ad libitum Purina rat chow powder, while the experimental group was fed ad libitum the rat chow powder blended with a mixture of four known free radical scavengers: allopurinol, mercaptopropionylglycine, dimethylthiourea and Vitamin E. A third group was pair-fed 10 g chow powder/rat/day, since in earlier experiments we observed that rats on the experimental diet consumed only about 10 g/rat/day. All rats were studied up to age 120 days. Body weight and food intake were measured daily. Urine was tested for glucose beginning at age 60 days. When glucosuria appeared, blood glucose and urinary ketones were measured. Body weight gain in the experimental and pair-fed groups was similar, but lower than the control group. Life table analysis of the data showed a decreased and a delayed onset of diabetes in the rats fed free radical scavengers. Thus, the results of this study demonstrated that calorie restriction and the related impaired growth did not affect the incidence of diabetes in the BB rat. In addition, the results suggested a role for free radicals in the spontaneous destruction of pancreatic beta-cells in the BB rat.
Diabetes Res Clin Pract 1992 Oct
PMID:Delayed onset and decreased incidence of diabetes in BB rats fed free radical scavengers. 144 73

Hemodynamic changes of lesser circulation were investigated in 108 patients with diabetic nephroangiopathy. They were also given vitamin E therapy (8 micrograms/kg of body mass) for 2 weeks to correct metabolic derangements and indices of pulmonary hemodynamics. Partial renal function was determined with 131I-hippuran and 99mTc-DTPA renoscintigraphy. Pulmonary hemodynamics was assessed with pulmonary scintigraphy (MAA 99mTc). The results have shown that vascular renal lesions in diabetes mellitus cause hypertension of lesser circulation and disorders in pulmonary microcirculation, and disorders of lipid metabolism and activation of lipid peroxidation (LPO) progress with augmentation of severity of disease. Vitamin E therapy improves pulmonary hemodynamics, lipid metabolism and LPO. Antioxidant correction was most effective at the initial stages of diabetic nephroangiopathy.
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PMID:[Disorders of pulmonary hemodynamics in patients with diabetic nephroangiopathy and its correction with antioxidants]. 151 66

Chronic vitamin E deficiency results in the premature and exaggerated development of neuroaxonal dystrophy (NAD) in primary sensory axon terminals in rat medullary gracile/cuneate nuclei, sites in which NAD develops normally with age. In the current study we determined if chronic Vitamin E deprivation had a similar effect on the development of NAD in the celiac/superior mesenteric sympathetic ganglia (C/SMG), another site with age-dependent NAD. The frequency of NAD failed to increase in the SMG of the same vitamin-E deficient animals in which a marked increase in severity of NAD was found in the gracile nucleus. These findings indicate that different populations of neurons are selectively involved in vitamin E deficiency and that the distribution of axonopathy in the E-deficient C/SMG does not duplicate the pattern of experimental diabetes and aging.
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PMID:Differential effect of chronic vitamin E deficiency on the development of neuroaxonal dystrophy in rat gracile/cuneate nuclei and prevertebral sympathetic ganglia. 206 45

Increased lipid peroxidation products were detected in a lipoprotein fraction containing very low density lipoprotein (VLDL) and low density lipoprotein (LDL) obtained from rats made diabetic by streptozotocin injection. The enhanced oxidation in the diabetic VLDL plus LDL fraction correlated with the in vitro toxicity of this lipoprotein fraction to proliferating fibroblasts. In contrast, high density lipoprotein (HDL) was not cytotoxic. That the increased oxidation and development of cytotoxic activity in the diabetic VLDL + LDL was related to the diabetes was shown by the fact that insulin treatment of diabetic animals inhibited both oxidation and cytotoxicity of VLDL + LDL. In contrast, treatment of diabetic rats with the antioxidants vitamin E or probucol after diabetes was established also inhibited both the in vivo oxidation and in vitro cytotoxicity of diabetic VLDL + LDL, but without altering hyperglycemia. Vitamin E or probucol treatment thus allowed separation of the oxidation process from the hyperglycemia occurring in experimental diabetes. The mechanisms by which diabetes in humans or experimental animals leads to the various manifestations of tissue damage are unknown; however, these studies demonstrate for the first time that a relationship exists between the in vivo oxidation of lipoproteins in diabetes and the potential for tissue damage as monitored by in vitro cytotoxicity. Furthermore, these results suggest that the mechanism for certain aspects of tissue damage accompanying experimental diabetes may be mediated by lipid peroxidation products.
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PMID:Antioxidant treatment of diabetic rats inhibits lipoprotein oxidation and cytotoxicity. 262 11

The effect of vitamin E (D-alpha-tocopherol acetate) on glycosylated hemoglobin levels was investigated in streptozotocin-diabetic rats. The animals were divided into four groups: (a) Group 1: control group, (b) Group 2: diabetic group, (c) Group 3: diabetic group treated with low-dose vitamin E and (d) Group 4: diabetic group treated with high-dose vitamin E. Starting 24 hr after streptozotocin injections (60 mg/kg), Groups 3 and 4 received intraperitoneal injections of vitamin E on days 1, 4, 7, 11, 14, 18 and 21 at doses of 500 mg/kg and 1,000 mg/kg respectively. Vitamin E treatment did not prevent weight loss or improve glycemic control in diabetic animals but significantly suppressed the increase in glycosylated hemoglobin in Group 4 (7.7 +/- 0.6 mumols fructose/g hemoglobin versus 5.5 +/- 0.2 mumols fructose/g hemoglobin in Group 2 and Group 4 respectively). These levels were still significantly higher than the levels in healthy control group animals (2.6 +/- 0.1 mumols fructose/g hemoglobin). Further studies on the suppressive effect of vitamin E are warranted.
Diabetes Res 1989 Nov
PMID:The effect of vitamin E on glycosylated hemoglobin levels in diabetic rats: a preliminary report. 263 93

An effect of vitamin E on blood platelets functioning was studied in 39 patients with diabetes mellitus type 1. Control group included 20 healthy blood donors. Vitamin E in a daily dose of 1000 mg produced statistically significant decrease in platelets aggregation, number of circulating platelet aggregates and release of the platelet factory 4 in diabetics after 7 days of treatment. No adverse reactions were seen in any patient treated with vitamin E. The obtained results indicate that vitamin E inhibits increased platelets activity in the patients with diabetes mellitus type 1 and does not exert toxic reactions during the treatment.
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PMID:[Effect of vitamin E on the function of blood platelets in patients with diabetes mellitus]. 270 39

High vitamin E supplementation in the diets of streptozocin-induced diabetic rats eliminates accumulation of lipid peroxides in the plasma and the liver, returns the plasma triglycerides toward normal levels, and increases the activity of lipoprotein lipase. Vitamin E has no effect on the levels of insulin or glucose. These findings suggest that vitamin E increases the total hepatic triglyceride lipase activity by increasing the lipoprotein lipase activity possibly by protecting the membrane-bound lipase against peroxidative damage.
Diabetes 1986 Mar
PMID:Triglyceride-lowering effect of dietary vitamin E in streptozocin-induced diabetic rats. Increased lipoprotein lipase activity in livers of diabetic rats fed high dietary vitamin E. 351 38

Weanling diabetes-prone BB rats were fed AIN-76 diets containing high (HE, 1 g/kg diet), basal (NE, 0.2 g/kg) or low (LE, trace) vitamin E and were killed at 21, 42 or 60 days of age. Plasma and tissues (adrenals, pancreas, spleen, thymus, liver, brown and white adipose tissue, muscle and testes) were analysed for vitamin E. Vitamin E levels reflected the level in the diet and no diabetic animals were detected at these times. In a second experiment, a total of 90 diabetes-prone BB rats were kept on diets LE and HE for 6 months or until they became diabetic. 11/45 on LE and 5/45 on HE became diabetic. Again, plasma and tissue levels of vitamin E reflected the levels in the diet with the exception of the thymus of diabetic rats fed the high vitamin E diet. Thymus vitamin E levels (microgram/g tissue) were 1.8 and 1.2 in LE-fed diabetics and asymptomatic rats, respectively; and 22.7 and 49.5 in HE-fed diabetics and asymptomatic rats, respectively. The last 2 values were significantly different (p less than 0.005). There were no other differences in plasma or tissue levels of vitamin E in these groups of animals. These findings suggest that high dietary vitamin E may decrease the incidence of diabetes in animals which are able to accumulate sufficient amounts of the vitamin in the thymus. Since the thymus plays a key role in the maturation of T cell populations, which appear to be altered in this disease, it seems possible that the protective effect may be exerted at this level.
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PMID:Effect of dietary vitamin E on the vitamin E status in the BB rat during development and after the onset of diabetes. 352 49

Vitamin E content and biosynthesis of 12-hydroxyeicosatetraenoic acid (12-HETE) have been measured in platelets from type I diabetic subjects and age- and sex-matched, nondiabetic control subjects. Platelets from diabetic subjects synthesized significantly greater quantities of 12-HETE than did platelets from control subjects when 12-HETE synthesis was induced by thrombin or collagen, either in the presence or absence of indomethacin. Platelet conversion of exogenously added arachidonic acid (AA) to 12-HETE was not significantly different between the diabetic and control groups in the absence of indomethacin, although a small but significant increase in the conversion of AA to 12-HETE was present in the diabetic group platelets when indomethacin was added to the reaction. Vitamin E content was significantly reduced in platelets from the diabetic subjects, when compared with platelets from the control subjects, although plasma vitamin E levels were not significantly different between the two groups. Thrombin- and collagen-induced platelet 12-HETE synthesis demonstrated a significant negative linear correlation with platelet vitamin E content when measurements from both diabetic and control groups were combined. The above data suggest a relationship between low vitamin E content and increased 12-HETE synthesis in platelets from type I diabetic subjects.
Diabetes 1985 Jun
PMID:Production of 12-hydroxyeicosatetraenoic acid and vitamin E status in platelets from type I human diabetic subjects. 392 90

Diabetic subjects tend to develop microvascular complications believed to be due to platelet hyperaggregability. This increased platelet sensitivity is though to be the result of an imbalance of PGI2 and TXA2 production in diabetes. This study sought to determine whether megavitamin E supplementation could restore PGI2/TXA2 balance in streptozotocin-diabetic rats. Endogenous release of PGI2 by isolated aorta, determined via radioimmunoassay of its stable metabolite, 6-keto-PGF1 alpha, was significantly greater (P less than 0.05) in rats receiving 100x the normal vitamin E requirement than in untreated diabetic rats. PGI2 synthesis was negatively correlated with plasma glucose levels (r = -0.87, P less than 0.05) in non-fasted rats at sacrifice. Vitamin E supplementation, at both the 10x and the 100x level, significantly depressed (P less than 0.05) thrombin-stimulated synthesis of TXA2 in washed platelet. PGI2 and TXA2 production were expressed as a ratio. Megavitamin E therapy appears to increase this ratio over that seen in the diabetic animal. The data suggest that vitamin E, at high levels, exerts an ameliorating influence of the PGI2/TXA2 imbalance of diabetes.
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PMID:Differential effects of megavitamin E on prostacyclin and thromboxane synthesis in streptozotocin-induced diabetic rats. 635 Jan 38


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