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)

Diabetic patients develop cardiomyopathy characterized mainly by left ventricular contractile dysfunction and congestive heart failure. This study has investigated the effects of diabetes and insulin treatment on lipid peroxidation, vitamin E, and vitamin E-quinone levels in the heart ventricles of rat made diabetic by streptozotocin treatment. Controls were injected with buffer alone; a subgroup of diabetic rats were injected daily with insulin for 2 months. Membrane lipid peroxidation was measured by determining the thiobarbituric acid (TBA)-reactivity. Vitamin E and vitamin E-quinone were measured by using the high pressure liquid chromatography. There was a significant (p < 0.02) increase in the vitamin E-quinone in the heart ventricles of diabetic rats (0.33 +/- 0.05 microgram/mg phospholipid) compared with control rats (0.19 +/- 0.02). This increase was prevented in insulin-treated diabetic rats (0.20 +/- 0.03). Vitamin E levels were higher (14.15 +/- 1.17 micrograms/mg phospholipid) in diabetic rats compared to control rats (9.93 +/- 1.29 (p < 0.03). However, insulin treatment to diabetic rats did not cause any change in vitamin E levels (11.75 +/- 1.02) compared with diabetic rats. TBA reactivity was higher in the heart ventricles of diabetic rats (1.09 +/- 0.11 nmole/mg phospholipid) compared with controls (0.78 +/- 0.08, p < 0.04). Insulin treatment to diabetic rats prevented the increase in the lipid peroxidation (0.79 +/- 0.07); there were no statistically significant differences in TBA-reactivity levels in heart ventricles of insulin-treated diabetic and control rats. This study documents accumulation of vitamin E-quinone and lipid peroxidation products in heart ventricles in diabetic rats, which may have a role in the altered contractile property of the heart ventricles in diabetes.
 ...
PMID:Elevated lipid peroxidation and vitamin E-quinone levels in heart ventricles of streptozotocin-treated diabetic rats. 774 18

The specific activities of superoxide dismutase, catalase, and glutathione S-transferase (mu subtype) were significantly lower in the brains of mice with type II diabetes than in the brains of control mice. On the other hand, the specific activity of glutathione peroxidase was unaltered. The concentration of vitamin E, but not that of total glutathione and ascorbate, was increased in the brains of the type II diabetic mice. The relative amount of polyunsaturated fatty acids (as determined with soybean lipoxygenase) was increased in whole brains and crude synaptosomal membranes of the type II diabetic mice. Endogenous levels of thiobarbituric acid-positive material were decreased in both whole brain homogenates and crude synaptosomal membranes of the db/db mice. Susceptibility of lipids within whole brain homogenates and crude synaptosomal membranes of mice with type II diabetes to peroxidation with iron/ascorbate was also markedly decreased compared with that of controls. Vitamin E is known to quench lipid peroxidation. Therefore, decreased lipid peroxidation in the type II mouse brain may be due to increased vitamin E content.
 ...
PMID:Antioxidant defense systems in the brains of type II diabetic mice. 779 Aug 73

Vitamin E was administered to non-obese diabetic (NOD) mice to determine if the selective destruction of pancreatic beta cells leading to Type 1 (insulin dependent) diabetes mellitus could be halted by virtue of this vitamin's free oxygen radical scavenger activity. Two groups of NOD mice were treated from 3 weeks of age until 30 weeks of age with either diet supplemented with vitamin E or control diet. Diabetes incidence was recorded as well as the degree of lymphocytic infiltration of the pancreas (insulitis) in animals which did not develop diabetes. Vitamin E did not reduce the incidence of diabetes by 30 weeks of age, however it did significantly delay the onset of the disease (p < 0.01--parallelism test). There were no differences in the degree of insulitis with respect to control mice. We conclude that antioxidant therapy with Vitamin E delays diabetes onset in NOD mice without having an apparent effect on the autoimmune process.
 ...
PMID:Vitamin E delays diabetes onset in the non-obese diabetic mouse. 785 66

Free radicals have been implicated in the development of diverse diseases such as cancer, diabetes, and cataracts, and recent epidemiological data suggest an inverse relationship between antioxidant intake and cardiovascular disease risk. Data also suggest that antioxidants may delay aging. Research has indicated that free radical production and subsequent lipid peroxidation are normal sequelae to the rise in oxygen consumption with exercise. Consequently, antioxidant supplementation may detoxify the peroxides produced during exercise and diminish muscle damage and soreness. Vitamin E, beta carotene, and vitamin C have shown promise as protective antioxidants. Other ingestible products with antioxidant properties include selenium and coenzyme Q10. The role (if any) that free radicals play in the development of exercise-induced tissue damage, or the protective role that antioxidants may play, remains to be elucidated. Current methods used to assess exercise-induced lipid peroxidation are not extremely specific or sensitive; research that utilizes more sophisticated methodologies should help to answer many questions regarding dietary antioxidants.
 ...
PMID:Free radicals, exercise, and antioxidant supplementation. 798 56

This study was performed to determine whether vitamin E supplementation in streptozotocin-induced diabetic rats treated by insulin could reduce serum oxidation markers (malondialdehyde: MDA, Schiff bases, anti-protein-MDA adduct antibodies) and modulate lipid changes. After 10 weeks, diabetes induced in rats a significant increase in Schiff bases (P < 0.006) and anti-protein-MDA adduct antibodies (P < 0.01). These alterations were accompanied by a significant rise in serum free fatty acids (225%), triglycerides (35%), and phospholipids (30%) and changes in fatty acid distribution in these fractions and in cholesterol esters. Vitamin E supplementation in diabetic rats reduced Schiff bases and anti-protein-MDA adduct antibodies and tended to restore the fatty acid profile close to control rats without decreasing quantitatively serum lipids enhanced by diabetes. Concerning fatty acids, vitamin E chiefly reduced stearic acid (C18:0) in free fatty acids, cholesterol esters, and phospholipids and cancelled the decrease in low molecular triglycerides observed in diabetic rats. Furthermore, vitamin E maintained the ratio of monounsaturated and polyunsaturated fatty acids, particularly with respect to oleic acid (C18:1), dihomo-gamma-linolenic acid (C20:3 n-6), eicosapentaenoic (C20:5 n-3), and docosapentaenoic acid (C22:5 n-3), in serum phospholipids. These changes observed in vitamin E supplemented rats, compared to vitamin E-untreated diabetic rats, could favor prevention of accelerated atherogenesis. Particularly, the decrease of serum peroxides and enhancement in phospholipid fatty acids (C20:3 n-6, C20:5 n-3, and C22:5 n-3) could induce the preferential formation of prostaglandins (PGE1, PGI2, PGI3) which are protective in cardiovascular diseases.
 ...
PMID:High dosage vitamin E effect on oxidative status and serum lipids distribution in streptozotocin-induced diabetic rats. 812 91

Premature atherosclerosis and other vascular disorders are serious complications of diabetes mellitus. Contributing factors include (i) increased peroxidation of LDL leading to foam cell formation, fatty streaks and plaque formation in the arterial wall, and (ii) hyperreactivity of blood platelets leading to increased platelet adhesion and aggregation. Vitamin E may play a protective role as an antioxidant and/or membrane stabilizing agent in either mechanism. In platelets it appears to regulate arachidonic acid metabolism. Decreased vitamin E levels in platelets are associated with increased aggregation. This is reversible by correction of the vitamin E status. In diabetics, platelet vitamin E levels tend to be reduced with concomitant increase in platelet aggregation. Several studies in patients with insulin-dependent diabetes mellitus and, to some extent, in those with non-insulin-dependent diabetes mellitus have shown that supplementation with several hundred IU vitamin E significantly reduced platelet aggregation and lipid peroxidation. In healthy volunteers high-dose supplementation had no notable effect on platelet aggregation. However, doses as low as 200 IU vitamin E significantly reduced platelet adhesion and inhibited the formation of protruding pseudopods typically occurring in activated platelets. In diabetic patients a decrease in the nonenzymatic glycation of proteins by vitamin E supplementation has been observed. Controlled studies are needed to confirm the effect of vitamin E on platelet function in well-defined groups of diabetics, followed by large-scale trials investigating the prevention of diabetic vascular complications as clinical end point.
 ...
PMID:Prevention of platelet dysfunction by vitamin E in diabetic atherosclerosis. 812 46

Patients with diabetes mellitus have an increased risk of thrombosis and accelerated atherogenesis. Increased platelet adhesion and aggregation are noted in vitro. This paper reviews known platelet abnormalities found in patients with diabetes mellitus (DM) and examines the pathophysiology associated with these abnormalities. Four general platelet regions or functional units can be involved in aberrant chemistry, structure and/or function. These include (1) the membrane, (2) granules, (3) intermediary metabolism, and (4) other factors and/or platelet responses to various substances. In regard to the abnormalities of the membrane, there is an increased binding of fibrinogen in diabetic rats and increased membrane rigidity. There are increases in glycoprotein Ib and glycoprotein IIb/IIIa. Related to granule function, increased levels of plasma serotonin, histamine and beta thromboglobulin are found. Alterations of intermediary metabolism involving the prostaglandin pathways, arachidonic acid, Vitamin E, and lipids have been reported. Other factors which are not well characterized include abnormalities of stem cell response to growth factors and thrombopoiesis, as noted indirectly through alterations of platelet volumes. It is proposed that these platelet abnormalities result in increased thrombosis and/or an acceleration of the atherosclerotic process in at least some patients with diabetes mellitus.
 ...
PMID:Platelet abnormalities in diabetes mellitus. 843 Oct

Free radicals have been suspected to play a role in the pathogenicity of alcohol-related chronic pancreatitis. The aim of this study was to determine the status of several antioxidant parameters in these patients and examine the factors that are likely to influence them. Thirty-five subjects (23 males and 12 females, mean age 48 +/- 8 years) with disease proven by endoscopic pancreatography and 14 healthy controls (6 males and 8 females, mean age 44 +/- 7 years) were included in the study. Biochemical antioxidant parameters included: selenium, zinc, and copper levels in plasma; glutathione peroxidase in plasma and erythrocytes; plasma malondialdehyde concentrations assessed by thiobarbituric acid reactants; and serum vitamin E and A levels. Selenium and vitamin E oral intake was assessed by a five-day diet analysis. Hemoglobin (130 +/- 16 vs 143 +/- 15 g/liter), vitamin E (8 +/- 5 vs 16 +/- 9 mg/liter), vitamin A (30 +/- 11 vs 49 +/- 12 micrograms/dl), selenium (54 +/- 20 vs 87 +/- 11 micrograms/liter), and plasma glutathione peroxidase (903 +/- 313 vs 1326 +/- 168 units/liter) were significantly lower in patients than in controls (P < 0.05). In contrast, white blood cell count, C-reactive protein, and plasma copper levels were significantly higher in patients than in controls. Cholesterol, triglycerides, iron, ferritin, total proteins, zinc, and malondialdehyde were not different. Vitamin E was lower in patients with steatorrhea, while vitamin A was lower in patients with concomitant diabetes mellitus. Dietary intakes were not different between patients and controls. In conclusion, patients with alcohol-related chronic pancreatitis have low blood levels in many antioxidant factors. Dietary intakes of some of them (selenium and vitamin E) are adequate, however. Such deficiencies are secondary to pancreatic insufficiency and probably to increased requirements related to enhanced oxidative stress.
 ...
PMID:Deficiency in antioxidant factors in patients with alcohol-related chronic pancreatitis. 865 56

Several lines of evidence support an atherogenic role for oxidized low-density lipoprotein (LDL). Previous studies have suggested that although Mexican-Americans have an increased rate of diabetes, obesity, elevated triglyceride levels, and low high-density lipoprotein (HDL) cholesterol levels, their rates of coronary heart disease (CHD) are similar or possibly lower than in non-Hispanic whites. Mexican-Americans have smaller, denser LDL than non-Hispanic whites. On the basis of this latter observation, we postulated that lipid peroxide (LPO) levels would be increased in Mexican-Americans. We examined the oxidizability of plasma in 50 Mexican-Americans and 50 non-Hispanic whites from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease, at baseline and after coincubation with a metal-independent system (2'2'-azobis-2-amidinopropane hydrochloride [AAPH]) and a metal-dependent system (Fe2+/H2O2) of oxidation. LPO levels were measured by a modified fluorimetric assay. Vitamin E and plasma fatty acid composition were also determined. We found significantly higher LPO levels at baseline and after AAPH coincubation in Mexican-Americans than in non-Hispanic whites (baseline, 2.75 +/- .09 v 2.07 +/- .09 micromol/L, P < .001; post-AAPH, 5.49 +/- .14 v 5.07 +/-. .04 micromol/L, P = .037). However, no significant ethnic differences were seen after coincubation with Fe2+/H2O2. Diabetes and cigarette-smoking were also associated with higher LPO levels. Mexican-Americans also had lower levels of vitamin E (the predominant lipid-soluble antioxidant in plasma) than non-Hispanic whites, although these differences only partially explained the differences in susceptibility to oxidation. Plasma fatty acids were similar in Mexican-Americans and non-Hispanic whites, suggesting only small differences in diet composition. We conclude that LPO levels are higher in Mexican-Americans than in non-Hispanic whites, and that these results are only partially related to differences in vitamin E levels.
 ...
PMID:Plasma oxidizability in Mexican-Americans and non-Hispanic whites. 869 25

Among many factors, elevated lipids and lipid peroxide levels in blood are major risk factors in the development of cardiovascular disease in diabetic patients. This study has examined whether oral supplementation of vitamin E, an antioxidant, has any effect on blood lipid peroxidation products (LP) and lipid profile of diabetic patients. Thirty-five diabetics(D) were supplemented with DL-alpha-tocopherol (E) capsule (orally, 100 IU/d) or placebo (P) for three months in double-blind clinical trials. Plasma E was analyzed by HPLC and LP by the thiobarbituric acid-reactivity; serum lipids by auto-analyzer. Data were analyzed using paired t-test and Wilcoxon Signed Rank Test. Vitamin E supplementation significantly lowered LP and lipid levels in diabetic patients; there were no differences in these parameters after P supplementation. There were no differences in the duration of diabetes and ages of D between P- and E- supplemented groups. This study suggests that vitamin E supplementation significantly lowers blood LP and lipid levels in diabetic patients.
 ...
PMID:The effect of modest vitamin E supplementation on lipid peroxidation products and other cardiovascular risk factors in diabetic patients. 872


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>