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

I have encountered 50 patients with clinical thrombophlebitis involving the lower extremites, with or without associated edema and pulmonary embolism, in whom longstanding self-medication with large amounts of vitamin E appeared to be a significant factor. The majority improved following cessation of vitamin E. In view of the epidemic nature of thrombophlebitis and deep vein thrombosis in the United States, the presumed innocuousness of vitamin E therapy requires reevaluation. Other clinical side effects also have been noted in patients receiving large doses of vitamin E. They include breast tenderness, elevation of blood pressure, a fatigue syndrome, myopathy, intestinal cramps, urticaria, and the possible aggravation of diabetes mellitus. The influence of concomitant metabolic, endocrine, and cardiovascular disorders on the thrombogenic potential of vitamin E is raised, and several possible mechanisms conducive to thrombophlebitis are reviewed.
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PMID:Thrombophlebitis associated with vitamin E therapy. With a commentary on other medical side effects. 43 74

Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 wk. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 or 8 wk. The control groups comprised rats not injected with STZ and fed either Mn-deficient or Mn-sufficient diets for a total of 12 wk. The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in the non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Plasma and hepatic vitamin E levels increased progressively with the duration of diabetes, independent of dietary Mn intake. Lipid peroxidation, as measured by H2O2-induced production of thiobarbituric acid reactive substances in erythrocytes, also increased, concomitant with decreased liver and kidney glutathione (GSH) levels. These findings demonstrate for the first time and interactive effective between Mn deficiency and STZ-diabetes, resulting in amplification of tissue antioxidant changes seen with either Mn deficiency or STZ-diabetes alone. This effect of Mn deprivation in experimental diabetes suggests a physiological role for Mn as an antioxidant nutrient.
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PMID:Tissue antioxidant status in streptozotocin-induced diabetes in rats. Effects of dietary manganese deficiency. 128 89

Tocopherol has been shown to have antiplatelet effects in insulin-dependent diabetes mellitus. However, its antiplatelet effect in non-insulin-dependent diabetes mellitus (NIDDM) remains to be established. In this report, the antiplatelet effect of tocopherol was assessed in a randomized, double-blind and crossover study of 15 NIDDM subjects. Each subject received tocopherol (dl-alpha-tocopherol nicotinate, 200 mg, tid) and a placebo for two six-week treatment periods separated by a three-week period in between for wash-out. The mechanisms of the antiplatelet effect of tocopherol were also studied in vitro. A significant decrease in platelet reactivity was observed after tocopherol treatment as compared with the pretest, and the magnitude of the decrease during tocopherol treatment was significantly evident when compared with that of the placebo treatment, as assessed by collagen (5, 10 micrograms/mL)-induced platelet aggregation of whole blood. A dose-dependent reduction in both ADP-and collagen-induced platelet aggregation was observed with tocopherol from 0.1 to 3.0 mM in vitro. No corresponding changes in ATP secretion and thromboxane synthesis were observed. Tocopherol also significantly inhibited fibrinogen-induced aggregation of elastase-treated platelets at a concentration of 0.1 mM. We demonstrated that platelet aggregation of whole blood ex vivo, among 15 NIDDM subjects was suppressed in tocopherol treatment, so tocopherol may have an antiplatelet effect in NIDDM subjects. The inhibitory effect of the platelet aggregation of tocopherol may be partially accomplished through interference with fibrinogen binding towards its receptor.
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PMID:Effect of tocopherol on platelet aggregation in non-insulin-dependent diabetes mellitus: ex vivo and in vitro studies. 135 87

The paper reviews published data on the products of platelet lipid peroxidation, their role in blood coagulation as other physiological and pathological processes. The authors discuss the significance of anti-oxidants (selenium, glutathione peroxidase, reduced glutathione and vitamin E) in removing excessive hydroperoxides and thus in the control of platelet functional activity. Changes in platelet arachidonic acid metabolites and in antioxidants were found in a number of pathological conditions such as diabetes mellitus and cardiovascular diseases.
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PMID:[Blood platelets, lipid peroxidation and antioxidants]. 147 66

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

Studies from several laboratories suggest that oxidized LDL may play an important role in atherogenesis. Our group previously showed that treatment of aortic endothelial cells with low levels of MM-LDL caused increased expression of MCP-1, M-CSF, tissue factor, and a monocyte-binding protein. In these studies MM-LDL was produced by storage of native LDL. We now show that cocultures of endothelial and smooth muscle cells can also produce MM-LDL from native LDL. This production of MM-LDL by cells is prevented by preincubating the LDL with probucol or vitamin E. However, addition of antioxidants to MM-LDL did not block its action. In past studies we also showed that endothelial cells exhibit differential sensitivity to the effects of MM-LDL. We report herein that in resistant cells there is no elevation of catalase, glutathione peroxidase, or copper-zinc-dependent SOD. However, manganese-dependent SOD is elevated in resistant cells. Ways in which MM-LDL production may be elevated in poorly controlled diabetics subjects are discussed.
Diabetes 1992 Oct
PMID:Minimally modified lipoproteins in diabetes. 152 40

The incidence of diabetes was reduced in non-obese diabetic (NOD) mice fed a diet containing 1000 IU/kg of vitamin E. Histologic examination of the islets of these mice, however, disclosed a frequency of insulitis that approximated the frequency found in animals fed conventional diets. The vitamin E-treated mice were not immunosuppressed, as judged by normal T cell subsets in the spleen and normal T cell proliferative responses to concanavalin A. NOD mice deprived of vitamin E were also protected from diabetes. However, these mice had delayed growth, reduced T cell numbers in the spleen, and impaired proliferative responses to mitogens, which is indicative of secondary immunodeficiency. The data are consistent with the view that antioxidant treatment may limit immunologically mediated damage to islet beta cells.
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PMID:Vitamin E supplementation reduces the incidence of diabetes but not insulitis in NOD mice. 158

Lipid peroxidation and the antioxidant status were studied in male patients having stable angina (SA) and unstable angina (UA) pectoris and the results were compared with that of controls. Lipid peroxides (LPx) and conjugated dienes (CD) were found to be elevated in patients with both SA (LPx: 3.96 +/- 1.07, P less than 0.001; CD: 357.09 +/- 66.23, P less than 0.01) and UA (LPx: 4.66 +/- 1.33, CD: 373.33 +/- 49.82, P less than 0.001) than in controls (LPx: 3.22 +/- 0.86, CD: 335.15 +/- 60.27). In SA, the erythrocytes expressed a diminished activity of superoxide dismutase (SOD) (SA: 435.59 +/- 76.02, control: 651.69 +/- 145.90, P less than 0.001) and normal activities of catalase and glutathione peroxidase, whereas in UA it showed enhanced activities of both SOD (UA: 735.72 +/- 145.67, P less than 0.01) and catalase (UA: 21.94 +/- 6.26, control: 18.69 +/- 6.37, P less than 0.01). A significant increase was also noticed in the levels of ceruloplasmin and vitamin E during both types of angina, but not alteration was observed in the levels of transferrin. Further, the patients with diabetes showed maximum levels of lipid peroxides compared to smokers and hypertensives. The level of lipid peroxides was also observed to increase with the severity of disease. This study indicates that free radicals are involved in the pathogenesis and progression of atherosclerotic heart disease.
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PMID:Antioxidant status in relation to free radical production during stable and unstable anginal syndromes. 163 72

Reduced prostacyclin (PGI2) production by the vascular wall may play an important role in the pathogenesis of vascular lesions such as atherosclerosis. The present study was undertaken to evaluate the effect of vitamin E on the production of PGI2 and other prostaglandins (prostaglandin E2 [PGE2], thromboxane A2 [TXA2], and 15-hydroxyeicosatetraenoic acid [15-HETE]) by bovine aortic endothelial cells cultured in a high concentration of glucose (300 mg/dL). Compared with endothelial cells cultured in 100 mg/dL glucose, the production of PGI2 and other prostaglandins, except 15-HETE, was significantly reduced in cultures containing 300 mg/dL glucose when stimulated by histamine, the Ca2+ ionophore, A23187, or human plasma-derived serum (PDS). The addition of vitamin E to each stimulant significantly restored the production of PGI2, PGE2, and TXA2, products of the cyclo-oxygenase pathway, in aortic endothelial cells cultured in 300 mg/dL glucose. This effect of vitamin E on the stimulation of prostaglandin production was generally specific for D-alpha-tocopherol, but not for the other vitamin E analogs tested. However, vitamin E and the stimulants had no effect on the production of 15-HETE, a product of the lipoxygenase pathway. Moreover, vitamin E alone, without stimulants, did not affect prostaglandin production in cultured bovine aortic endothelial cells. These results suggest that vitamin E may restore reduced PGI2, PGE2, or TXA2 production by bovine aortic endothelial cells cultured in a high concentration of glucose. It seems likely that vitamin E may restore depressed PGI2 production by the vascular wall in hyperglycemic conditions such as those seen in patients with diabetes mellitus.
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PMID:Vitamin E restores reduced prostacyclin synthesis in aortic endothelial cells cultured with a high concentration of glucose. 164 Aug 48

It is known that plasma low density lipoproteins (LDL) contain a great amount of vitamin E and that LDL enter cells via the specific receptor-mediated mechanism. In this study, we aimed to investigate the transport of alpha-tocopherol from plasma to tissues in subjects with non-insulin-dependent diabetes mellitus (NIDDM) with poor glycaemic control; and the relationships between alpha-tocopherol and plasma lipid and lipoprotein levels. alpha-Tocopherol determination was carried out by colorimetric assay according to the modified micromethod of Fabianek et al. The mean plasma alpha-tocopherol and (LDL + VLDL)-alpha-tocopherol levels increased significantly in the diabetic group as compared to control (P less than 0.05 and P less than 0.02), whereas the high density lipoprotein (HDL)-alpha-tocopherol level was significantly lower in the diabetic group than that in the controls (P less than 0.05). Correlations between plasma alpha-tocopherol levels showed close positive relationships (r = 0.87, r = 0.75 and r = 0.78, respectively, P less than 0.001). A strong positive correlation was also observed between alpha-tocopherol and the cholesterol content, either in the HDL or in the (LDL + VLDL) fractions (r = 0.75 and r = 0.77; P less than 0.001). These findings indicate that there is a direct positive relationship between lipid and alpha-tocopherol concentrations. The increased level of alpha-tocopherol in the LDL + VLDL fraction and decreased level in HDL in these patients could be attributed to the impairment of the cholesterol uptake of the cells by the receptor mediated mechanism.
Diabetes Res Clin Pract 1991 Dec
PMID:The transport of vitamin E in plasma and its correlation to plasma lipoproteins in non-insulin-dependent diabetes mellitus. 177 10


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