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

Platelet vitamin E content and thromboxane A2 (TxA2) synthesis have been investigated in type I diabetic subjects and age- and sex-matched controls. Platelets, but not plasma, from diabetic subjects contained significantly lower vitamin E levels and synthesized significantly greater amounts of TxA2 when challenged with collagen or thrombin than platelets from control subjects. Conversion of exogenously added arachidonic acid to TxA2 was unaltered between platelets from control and diabetic groups. Platelet vitamin E content from control and diabetic groups combined exhibited a significant negative linear correlation with collagen- and thrombin-induced TxA2 production. These data suggest that low platelet vitamin E levels could be a contributing factor to the increased thromboxane synthesis demonstrated by platelets from the above type I diabetic subjects.
Diabetes 1984 Mar
PMID:Interrelation of platelet vitamin E and thromboxane synthesis in type I diabetes mellitus. 669 15

Measurement of lipid peroxides and alpha-tocopherol was undertaken in rats with streptozotocin-induced diabetes. In sera and livers in diabetic rats, the lipid peroxides increased but alpha-tocopherol decreased. To study the effect of vitamin E deficiency in the diabetic state, diabetes was induced in rats maintained on a vitamin E deficient diet. Serum lipid peroxides increased greatly but alpha-tocopherol decreased. Lipid peroxides and alpha-tocopherol increased in the liver of vitamin E deficient states. In the liver, vitamin E deficient diabetic rats had lower lipid peroxides levels but higher alpha-tocopherol levels than vitamin E deficient non-diabetic rats. On the basis of the present experiments, it was considered that the decrease of alpha-tocopherol might be due to consumption as an antioxidant as lipid peroxides increased in sera and livers. The decrease of lipid peroxides in the liver was thought to play an important part of the increase in serum lipid peroxides.
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PMID:Lipid peroxides and alpha-tocopherol in rat streptozotocin-induced diabetes mellitus. 711 41

In 43 diabetes mellitus patients and 15 normal individuals, the vesicular and liver portions of the bile were subjected to clinical and laboratory studies for macro- and microscopic bile characteristics, the content of chelates, cholesterol, bilirubin, activity of aspartic and alanine aminotransferases before and after inclusion of vitamin E into combined therapy. It was established that vitamin E has a favourable effect on liver function and it is thus desirable to include it into combined therapy of liver injuries in diabetes mellitus patients.
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PMID:[Effectiveness of vitamin E in the combined therapy of the hepatobiliary system lesions in diabetes mellitus]. 715 41

Experimental study of liver function in male white rats with alloxan diabetes has shown that vitamin E in a dose of 10 mg per 100 g body weight reduces the animals death and intoxication, and speeds up the recovery of liver function. The drug improves excretion of cholates with bile, exerts a beneficial effect on cholesterol and bilirubin secretion with bile.
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PMID:[Effect of vitamin E on the secretion and chemical composition bile in alloxan diabetic Rats]. 724 93

We studied the effect of supplementation with vitamins C, E and beta-carotene (PARABION, produced by Syndipharma) on antioxidative status in kidneys of male Wistar rats with diabetes induced by intravenous application of streptozotocin (45 mg.kg-1 of body weight). The animals received subtherapeutic doses of Insulin Interdep (6 U.kg-1 of body weight). A significant decrease of malondialdehyde (MDA), reduced (GSH) and oxidized (GSSG) glutathione and reduction of the activities of Se-glutathione peroxidase (Se-GSH-PX, EC. 1.11.1.9.) and glutathione S-transferase (GST, EC. 2.5.1.18.) were observed in kidneys of diabetic rats treated with these vitamins. On the contrary, the activity of CuZn-superoxide dismutase (CuZn-SOD, EC. 1.15.1.1) and the level of vitamin C (vit. C) increased significantly. No changes were observed for vitamin E (vit. E), beta-carotene and catalase (CAT, EC. 1.11.1.6). Supplementation with vitamins C, E and beta-carotene resulted in an improvement of antioxidative status of kidneys of rats with streptozotocin-induced diabetes.
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PMID:Effect of intake of exogenous vitamins C, E and beta-carotene on the antioxidative status in kidneys of rats with streptozotocin-induced diabetes. 747 41

Persons with diabetes are at increased risk for developing coronary heart disease (CHD): although the standard risk factors are also applicable, there are other major nontraditional risk factors for these persons. For example, oxidation of lipoproteins may play an important role in the development of atherosclerosis. Another risk factor is the presence of small, dense low-density lipoprotein (LDL), which may have enhanced atherogenicity because it enters the arterial wall more readily and is more easily oxidized. Both of these factors may be particularly important in persons with non-insulin-dependent diabetes mellitus (NIDDM), because these persons may have greater rates of lipid oxidation in vivo than do nondiabetic persons and also have an increased prevalence of small, dense LDL. I describe potential dietary and pharmacologic regimens in patients with NIDDM to decrease in vivo lipid peroxidation, and the susceptibility of LDL and dense LDL subfractions to oxidative modification. In nearly all NIDDM patients, reducing dietary saturated fat helps lower plasma cholesterol and reduces the risk for CHD. There is, however, some controversy as to whether dietary saturated fat should be replaced by carbohydrates or by monounsaturated fatty acids (MUFAs) in NIDDM. Recent studies showed reduced susceptibility to oxidation of LDL in subjects consuming MUFA-enriched diets, thus adding another dimension to the ongoing debate over the most appropriate diet for NIDDM patients. Additionally, supplemental antioxidants such as probucol and vitamin E alone or in combination with MUFA-enriched diets have shown promise in protecting LDL from oxidation when given to nondiabetic populations. I also present recent results from an antioxidant trial in NIDDM subjects.
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PMID:Dietary and pharmacologic regimens to reduce lipid peroxidation in non-insulin-dependent diabetes mellitus. 749 49

The prevalence of coronary artery disease (CAD) in the urban population of India is similar to that in developed countries; Indian immigrants in industrialized countries have the highest prevalence of CAD. This is a cross-sectional survey within a random sample of a single urban setting in India. The relation between risk of CAD and plasma levels of vitamins A, C, E, and beta-carotene was examined in 72 of 595 elderly subjects (12.1%) with CAD (aged 50 to 84 years). Plasma levels of vitamins A, C, E, and beta-carotene were significantly related to risk of CAD. Smoking (n = 145) and diabetes (n = 70) were the confounding factors. Lipid peroxides were higher in patients with CAD and diabetes, and in those who smoked. The inverse relation between CAD and low plasma vitamin C was substantially reduced after adjustment for smoking and diabetes. Vitamin A and E levels remained independently and inversely related to the risk of CAD after adjustment for age, smoking, diabetes, blood pressure, blood lipoproteins, and relative weight and body mass index. The adjusted odds ratios for CAD between the lowest and highest quintiles of vitamin E levels were 2.53 (95% confidence interval [CI] 1.11 to 5.31), vitamin C, 2.21 (95% CI 1.12 to 3.15), and beta-carotene, 1.72 (95% CI 0.88 to 3.62). The fatty acid composition of the diet, blood lipid levels, central obesity (waist-hip ratio), smoking habits, blood pressure, and plasma insulin levels do not appear to account for high rates of CAD among elderly Indians.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary intake, plasma levels of antioxidant vitamins, and oxidative stress in relation to coronary artery disease in elderly subjects. 750 2

We examined the effect of two endogenous antioxidant agents, taurine and vitamin E, on renal function in experimental diabetes. Male Sprague-Dawley rats, rendered diabetic with streptozocin (STZ), were assigned to one of the following groups: 1) untreated; 2) insulin treatment with 6 U Ultralente insulin/day in two doses; 3) taurine supplementation by 1% taurine in drinking water; and 4) vitamin E supplementation at 100 IU vitamin E/kg chow. Animals were kept for 52 wk. The survival rate was similar (70-90%) in all groups except vitamin E-treated animals, of which 84% died by 6 mo. At 52 wk, glomerular filtration rate was elevated in untreated and taurine-treated STZ rats compared with normal or insulin-treated diabetic rats. Taurine supplementation reduced total proteinuria and albuminuria by nearly 50%. This treatment also prevented glomerular hypertrophy, preserved immunohistochemical staining for type IV collagen in glomeruli, and diminished glomerulosclerosis and tubulointerstitial fibrosis in diabetic animals. The changes in renal function and structure in taurine-treated diabetic rats were associated with normalization of renal cortical malondialdehyde content, lowering of serum free Fe2+ concentration, and decreased formation of the advanced glycooxidation products, pentosidine, and fluorescence in skin collagen. Administration of the vitamin E-enriched diet exacerbated the nephropathy in STZ-diabetic rats. In addition, vitamin E supplementation increased serum free Fe2+ concentration, enhanced renal lipid peroxidation, and accelerated the accumulation of advanced glycosylation end products (AGEs) in skin collagen. We conclude that administration of taurine, but not vitamin E, to rats with STZ-diabetes ameliorates diabetic nephropathy. The beneficial effect of taurine is related to reduced renal oxidant injury with decreased lipid peroxidation and less accumulation of AGEs within the kidney.
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PMID:Taurine ameliorates chronic streptozocin-induced diabetic nephropathy in rats. 757 92

We measured levels of plasma and milk alpha-tocopherol in women with insulin-dependent diabetes mellitus (IDDM), women without IDDM, and healthy reference women. Milk collections were made at 7, 14, 42, and 84 days postpartum; blood was collected at 3, 14, and 42 days. Postprandial glucose at 80 min was used to describe metabolic control of women with IDDM postpartum. There was no difference between the groups for plasma alpha-tocopherol, which was within normal reported levels. Tocopherol (micrograms/g lipid) decreased by approximately 50% in all groups between 7 and 14 days. The trend for milk tocopherol was similar when expressed as micrograms/dl. Metabolic control did not have a significant effect on mean milk or plasma alpha-tocopherol. We have shown that this group of women with IDDM produced a milk with vitamin E content similar to control and reference women. We conclude that the infant of the breast-feeding woman with IDDM who is in good metabolic control during pregnancy and who receives good prenatal counseling most likely receives adequate vitamin E from the mother's milk.
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PMID:Vitamin E in plasma and milk of lactating women with insulin-dependent diabetes mellitus. 760 25

Friedreich ataxia is an autosomal recessive ataxia with onset usually before puberty whose characteristic clinical features include progressive ataxia of gait and limbs, dysarthria, loss of joint position and vibratory sense, absent knee and ankle jerks, and Babinski signs. Foot deformity, scoliosis, diabetes mellitus, and cardiac involvement are common and characteristic. Patients survive until about age 30 years although longer survivals occur. A later onset, more slowly progressive form seems to be an allelic variant. The basic process seems to be a dying-back of neuronal processes. Using linkage mapping techniques, the classical form of Friedreich ataxia has been localized to 9q13-q21, a region on the long arm of chromosome 9. Haplotype analysis, analysis of recombinants, and physical mapping techniques, including construction of a YAC contig, have narrowed the interval for the Friedreich ataxia gene, FRDA, to a few hundred thousand base pairs. Candidate genes in the region are being studied by techniques of mutation analysis. It is likely that the Freidreich ataxia gene will be cloned soon. A condition resembling Friedreich ataxia with decreased vitamin E levels has been localized to chromosome 8 and is discussed elsewhere.
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PMID:Friedreich ataxia. 761 92


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