Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin E deficiency in erythrocytes causes decreased cell survival, hypercoagulability, and increased adhesiveness to the endothelium. Similar abnormalities are found in erythrocytes of the diabetic population. This study examines the effect of diabetes on vitamin E and lipofuscin products (aging pigments) in erythrocytes of streptozocin-induced diabetic rats. Controls were injected with buffer alone, and a subgroup consisting of insulin-treated diabetic rats were injected daily with insulin for 2 mo. Mean +/- SD vitamin E levels were 23.2 +/- 4.9, 19.4 +/- 3.2, and 25.9 +/- 2.5 nmol/mumol phospholipid. Lipid fluorescence values (relative values/phospholipid) were 11.1 +/- 1.9, 14.1 +/- 2.6, and 11.9 +/- 1.8 (excitation/emission 360/440 nm) in control, diabetic, and insulin-treated diabetic rats, respectively. Differences in vitamin E and lipofuscin products were significant between all control and diabetic groups and diabetic and insulin-treated diabetic groups. Reduction in vitamin E and increases in lipofuscin products in diabetic rats were significant even when values were expressed per micromole Hb or per 100 ml erythrocytes. This study demonstrates that hyperglycemia significantly reduces vitamin E and increases lipofuscin products in erythrocytes of diabetic rats. These effects were prevented with insulin treatment.
Diabetes 1991 Oct
PMID:Reduced vitamin E and increased lipofuscin products in erythrocytes of diabetic rats. 193 87

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.
 ...
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

Thirteen patients with adult-onset vitamin E deficiency due to fat malabsorption were investigated clinically and electrophysiologically. These patients had slightly or moderately decreased serum vitamin E (1.7-4.8 micrograms/ml, normal less than 6.0) or vitamin E/cholesterol ratio (0.21-0.31 mg/g, normal less than 0.35). Only one patient had typical neurological manifestations of vitamin E deficiency, which improved with supplementary vitamin E. The pathological findings in this patient were also compatible with vitamin E deficiency. This patient had poorly controlled diabetes mellitus due to advanced chronic pancreatitis. Reviewing previously reported cases of vitamin E deficiency with diabetes mellitus in chronic pancreatitis, the duration of deficiency until the onset of symptoms was shorter than in those cases without complications. Although adult patients with early, slight deficiency of vitamin E are generally asymptomatic, patients with diabetes mellitus tend to have early neurological symptoms. The vitamin E tolerance test should be used, because even in some patients with vitamin E deficiency due to malabsorption, the deficiency can be overcome by large oral doses of vitamin E.
 ...
PMID:Vitamin E deficiency in acquired fat malabsorption. 235 33

Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2 subfraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides; omega-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLch levels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
 ...
PMID:Nutritional management of plasma lipid disorders. 255 90

Vitamin E deficiency is associated with increased platelet aggregation, which can be normalized through vitamin E supplementation. In diabetes, increased platelet thromboxane A2 (TXA2) production is correlated with decreased platelet vitamin E content. We therefore investigated the effect of 400 mg DL-alpha-tocopherol acetate daily for 4 wk on ADP- and collagen-induced platelet aggregation and platelet TXA2 production in 22 type I (insulin-dependent) diabetic patients without macroangiopathy and with no or only minimal microangiopathy by a double-blind placebo-controlled crossover study. Platelet aggregation was induced in platelet-rich plasma by two or three different concentrations of ADP and collagen. TXA2 was measured by the stable spontaneous breakdown product thromboxane B2 by a specific radioimmunoassay. Whereas metabolic control remained unchanged during the study period, platelet TXA2 production was significantly (P less than .05 and P less than .01) reduced at each ADP concentration and at two of three collagen concentrations. Because increased TXA2 production of diabetic platelets is thought to play an important pathogenetic role in diabetic angiopathy, we conclude that vitamin E treatment could be beneficial with respect to platelet-vessel-wall interaction and thus might be promising for the prevention of diabetic angiopathy.
Diabetes 1988 Sep
PMID:Effect of vitamin E supplementation on platelet thromboxane A2 production in type I diabetic patients. Double-blind crossover trial. 304 91

The mechanisms and cardiovascular effects of omega-3 fatty acids are reviewed. Omega-3 polyunsaturated fatty acids are the major ingredient found in commercially available fish oil products. The incidence of many diseases, including coronary heart disease, diabetes mellitus, and psoriasis, is lower in Eskimos, who ingest diets rich in omega-3 fatty acids, compared with European controls. Potential mechanisms by which these fatty acids cause their many physiologic effects include competing with omega-6 fatty acids for prostaglandin and leukotriene pathways and enhancing cell membrane fluidity by virtue of the high degree of unsaturation. Numerous studies have documented longer bleeding times and decreased platelet aggregation in subjects ingesting omega-3 fatty acids. Omega-3 fatty acids may reduce serum cholesterol concentrations by decreasing the synthesis of very low density lipoprotein and, therefore, low-density lipoprotein. Blood viscosity is significantly and uniformly lower in subjects receiving omega-3 fatty acids compared with controls. Potential risks of supplementation with fish oils include hypervitaminosis A and D, vitamin E deficiency, increased bleeding times, decreased platelets, and ingestion of contaminated fish. Supplementation with moderate amounts of omega-3 fatty acids appears to be relatively safe. Possible adverse effects include nausea, diarrhea, and a "fishy" taste. Properly controlled, long-term clinical trials are needed to determine whether supplementation with omega-3 fatty acids would be therapeutically beneficial in various patient populations and disease states.
 ...
PMID:Biological mechanisms and cardiovascular effects of omega-3 fatty acids. 305 76

There is increasing evidence that islet beta cells may be susceptible to redox insult, and that this susceptibility may contribute to the pathogenesis of experimental models of diabetes mellitus. We investigated the effect of vitamin E deficiency, selenium deficiency, and combined deficiency on islet function and free radical scavenging systems. The tissue levels of glutathione peroxidase, catalase, and immunoreactive superoxide dismutases were measured in four groups of rats (i.e., controls and those with vitamin E, selenium, and combined deficiency). Glucose tolerance tests were performed for each animal before sacrifice. Superoxide dismutase concentrations in liver, heart, and skeletal muscle were within 20% of the control levels in all groups. However, the manganosuperoxide dismutase concentrations in islets were significantly lower than control levels in response to vitamin E, selenium, and combined deficiency. Combined deficiency appeared to have an additive effect. In contrast, cuprozinc superoxide dismutase concentration in islets was higher in the deficient groups than in controls. Insulin secretory reserve was decreased in each of the three deficient groups. This decrease was reflected as glucose intolerance only in the group with combined deficiency. Glutathione peroxidase activity was markedly decreased in selenium-deficient animals in all tissues studied. Catalase activity did not change significantly among groups in any tissue studied. Islets had the lowest glutathione peroxidase and cuprozinc and total superoxide dismutase levels among tissues studied.
 ...
PMID:Effect of vitamin E deficiency and selenium deficiency on insulin secretory reserve and free radical scavenging systems in islets: decrease of islet manganosuperoxide dismutase. 351 3

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.
 ...
PMID:Lipid peroxides and alpha-tocopherol in rat streptozotocin-induced diabetes mellitus. 711 41

The effect of streptozotocin-induced diabetes on the urinary excretion of thiobarbituric acid test-positive materials was examined. In diabetic rats, urinary excretion of thiobarbituric acid reactive substances was increased 5-fold over that in nondiabetic animals. High-performance liquid chromatography of urine samples revealed that five of the six fractions previously found to be increased in vitamin E deficiency [Lee, H.-S., Shoeman, D.W., and Csallany, A.S. (1992) Lipids 27, 124-128] were also significantly increased in streptozotocin-induced diabetes. The data suggest that a high level of oxidative stress is induced by uncontrolled diabetes in rats.
 ...
PMID:Diabetes increases excretion of urinary malonaldehyde conjugates in rats. 835 96

How much vitamin E is enough? An established use of supplemental vitamin E in humans is in the prevention and therapy of deficiency symptoms. The cause of vitamin E deficiency, characterized by peripheral neuropathy and ataxia, is usually malabsorption-a result of fat malabsorption or genetic abnormalities in lipoprotein metabolism. Genetic abnormalities in the hepatic alpha-tocopherol transfer protein also cause vitamin E deficiency-defects in this protein cause an impairment in plasma vitamin E transport. Impaired delivery of vitamin E to tissues, thereby, results in deficiency symptoms. Also discussed is the use of supplemental vitamin E in chronic diseases such as ischemic heart disease, atherosclerosis, diabetes, cataracts, Parkinson's disease, Alzheimer's disease, and impared immune function, as well as in subjects receiving total parenterol nutrition. In healthy individuals, a daily intake of about 15-30 mg of alpha-tocopherol is recommended to obtain "optimal plasma alpha-tocopherol concentrations" (30 microM or greater).
 ...
PMID:Vitamin E in humans: demand and delivery. 883 30


1 2 Next >>