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

Lipid peroxidation of liposome made of egg lecithin was induced by glucosone (D-arabino-hexos-2-ulose), a secondary product of Maillard reaction or glycation of protein. Lipid peroxidation was assessed with measurement of TBARS (thiobarbituric acid reacting substances), POV (peroxide value), and HPLC measurement of MDA (malondialdehyde). EDTA and DTPA (diethylenetriamine-pentaacetic acid) inhibited the lipid peroxidation assessed by each method described above, indicating involvement of metal ions. The observed reduction of Fe3+ to Fe2+ by glucosone might be a critical step of the lipid peroxidation. Our findings suggest a possible role of lipid peroxidation of low-density lipoproteins (LDL) induced by glucosone in atherosis caused by diabetes mellitus.
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PMID:Lipid peroxidation of liposome induced by glucosone. 129 43

The aim of this experiment was to study the interrelationships between nutritional status of chosen trace elements (Cu, Zn, Fe) and hepatic lipid peroxidation in streptozotocin-induced diabetic rats. Both copper accumulation and disruption of iron storage were observed in livers of diabetic rats. MDA 0' (baseline) and MDA 30' (produced) levels measured in the liver were negatively correlated with blood glucose levels. MDA 30' levels correlated positively with iron concentration in the liver. It is supposed that the hormonal lability during experimental diabetes caused changes in metabolism of trace elements, and subsequently influenced the rate of lipid peroxidation.
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PMID:Hepatic lipid peroxidation and trace elements--nutritional status in streptozotocin-induced diabetic rats. 149 28

In vitro studies have demonstrated that gliclazide has free radical scavenging and antiplatelet activities. To assess this clinically, we studied gliclazide in a blinded, randomized, glibenclamide-controlled trial in 30 type II diabetic patients with retinopathy. All patients had been taking glibenclamide for more than 12 months before being randomized to receive either an equipotent dose of gliclazide or to continue on glibenclamide. Diabetic control was not modified. The patients were well matched at randomization (mean age, 58 years; duration of diabetes, 8 years; 20 males; mean hemoglobin A1 [HbA1], 8.6%) and their degree of diabetic control was not altered during the trial. Free radical activity was assessed as oxidative status by plasma thiols (PSH), lipid peroxides (MDA-LM), and red blood cell superoxide dismutase activity (SOD). Platelet aggregation in whole blood to collagen (Plt-ag) was used as the measure of platelet reactivity. There were no differences between these measurements at baseline. At 3 months, the oxidative status and platelet aggregation in the gliclazide group had improved significantly compared with baseline and had also showed significant differences in all parameters when compared with the glibenclamide group. Therefore, comparing gliclazide with glibenclamide-treated patients at 3 months, we found: PSH, 458 +/- 38 versus 414 +/- 34 mumol/L, P less than .004; MDA-LM, 7.0 +/- 0.6 versus 8.3 +/- 0.8 mumol/L, P less than .0002; SOD, 152 +/- 36 versus 123 +/- 15 micrograms/mL, P less than .016; Plt-ag, 50.8 +/- 24 versus 72.3% +/- 15%, P less than .006. These changes were maintained at 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients: clinical assessment. 157 14

In non-insulin-dependent diabetes mellitus (NIDDM) patients, microalbuminuria predicts early mortality, predominantly from cardiovascular disease. Increased free radical activity and abnormalities in hemostasis have been implicated in the development of vascular disease. Therefore, we measured markers of free radical activity (nonperoxide-conjugated diene isomer of linoleic acid [PL-9,11-LA'] and lipid peroxides expressed as malondialdehyde [MDA]) along with the hemostatic variables: fibrinogen, von Willebrand factor (vWf), plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (t-PA), and plasmin activity (B beta 15-42) in 24 NIDDM patients (12 patients with microalbuminuria and 12 without microalbuminuria) and in 12 age-matched control subjects. There were no differences in linoleic acid (PL-9,12-LA) concentrations between the three groups. PL-9,11-LA' was elevated in the microalbuminuric patients compared with control subjects (P less than 0.05), but there was no difference between the two diabetic groups. MDA was elevated in the microalbuminuric diabetic patients compared with those patients without microalbuminuria (P less than 0.05) and control subjects (P less than 0.001). MDA was also increased in the patients without microalbuminuria compared with control subjects (P less than 0.01). Except for B beta 15-42, all the hemostatic variables were increased (P less than 0.05) in the diabetic patients compared with control subjects. The microalbuminuric diabetic patients had further increases in vWf (P less than 0.03) and t-PA (P less than 0.03) compared with patients with microalbuminuria. Our study suggests that there is an increase in free radical activity and abnormalities in hemostatic variables favoring a hypercoagulable state in NIDDM, especially in those with microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1992 Aug
PMID:Free radical activity and hemostatic factors in NIDDM patients with and without microalbuminuria. 162 64

An increase in oxidative stress may contribute to the development of diabetic complications. The key aqueous-phase chain-breaking antioxidant ascorbate is known to be deficient in diabetes, and we have therefore investigated the effects of ascorbate supplementation on oxidative stress in the streptozotocin diabetic rat. Markers of lipid peroxidation (malondialdehyde [MDA] and diene conjugates) were increased in plasma and erythrocytes of untreated diabetic animals, and levels of the antioxidants ascorbate and retinol were reduced. Plasma tocopherol was unchanged. Insulin treatment normalized MDA and ascorbate levels, although ascorbate metabolism remained disturbed, as indicated by increased levels of dehydroascorbate. High-dose ascorbate supplementation in the absence of insulin treatment restored plasma ascorbate to normal and increased plasma retinol and tocopherol levels. However, MDA and diene conjugate levels remained unchanged, possibly as a result of increased iron availability. High-dose ascorbate supplementation should be approached with caution in diabetes, as ascorbate may exert both antioxidant and prooxidant effects in vivo.
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PMID:The effect of ascorbate supplementation on oxidative stress in the streptozotocin diabetic rat. 162 52

To determine if experimental diabetes is associated with decreased antioxidative potential along with increased peroxidation of lipids in cerebral microvessels, streptozotocin-induced diabetic rats were compared with control rats and to diabetic rats treated with insulin. Isolated cerebral microvessels from diabetic rats had significantly higher concentrations of malondialdehyde (MDA; micrograms/mg protein) (0.0283 +/- 0.0017) compared with control (0.0201 +/- 0.0016) or insulin-treated diabetic rats (0.196 +/- 0.0022) P < 0.01. The antioxidative potential was measured in the presence of a peroxy radical generator 2,2'-azobis(2-amidinopropane) (AAPH) and hydroxyl radical generator CuSO4 with monitoring of the fluorescence of phycoerythrin at 37 degrees C. The free radical quenching activity of cerebral microvessels expressed as % inhibition of phycoerythrin oxidation by AAPH was significantly reduced in diabetic rats (38.7 +/- 4.5%) compared with control (54.3 +/- 4.9%) or insulin-treated diabetic rats (57.6 +/- 2.9%) (P < 0.01). The % inhibition of oxidation by cerebral microvessels in the presence of CuSO4 was only 15.7 +/- 3.1% and did not differ significantly in diabetic rats (13.1 +/- 2.1%). The results indicate that antioxidative potential of cerebral microvessels, especially in the presence of peroxy radical generator, is reduced in diabetes along with increased accumulation of lipid peroxidation byproducts. Increased oxidative stress may be one of the many mechanisms underlying the diabetes-related changes in the blood-brain barrier.
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PMID:The antioxidative potential of cerebral microvessels in experimental diabetes mellitus. 772 29

We assessed the effect of dipyridamole, RA-642 and mopidamol, on lenticular opacities in a model of experimental diabetic cataracts in rats. All three pyrimido-pyrimidine derivatives caused a statistically significant reduction of opacification in crystalline lens as compared with untreated diabetic animals. The production of superoxide anions (phenazine methosulphate [PMS]-induced nitroblue tetrazolium [NBT] reduction) showed a decrease of 81.6%, 78.9% and 1.8% in lens tissue homogenates from rats treated with dipyridamole, RA-642 and mopidamol, respectively. Dipyridamole and RA-642 produced a statistically significant inhibition (50% and 64.8%, respectively) of lipid peroxidation (ferrous sulphate and ascorbic acid [FeAs]-induced malondialdehyde [MDA] production) as compared with the group of untreated diabetic rats. Mopidamol did not exert any inhibitory effect on lipid peroxidation. There was a statistically significant correlation between opacification of lens and PMS-induced NBT reduction and FeAs-induced MDA production. We conclude that the protective effect of dipyridamole and RA-642 from free radical damage to crystalline lens in the model of experimental diabetes used in this study, is the result of the antioxidant action of these compounds. The effect exerted by mopidamol, however, suggest a possible complementary effect of the pyrimido-pyrimidine derivatives through interaction with other mechanisms (e.g., the sorbitol pathway) implicated in the development of cataracts.
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PMID:The pyrimido-pyrimidine derivatives, dipyridamole and RA-642, reduce opacification of crystalline lens in diabetic rats. 787 Jun 94

We have studied platelet aggregation and membrane fluidity, along with various biochemical parameters, in 19 non-insulin-dependent diabetes mellitus (NIDDM) patients prior to control of blood sugar, 11 patients after control of blood sugar, and 26 normal subjects. Platelet cholesterol: phospholipid ratio and basal levels of)[Ca+] were comparable between normal and uncontrolled NIDDM. Basal levels of malonaldehyde (MDA) and the levels of [Ca++]i, as well as MDA after the addition of arachidonic acid, were 2.5-fold, 5-fold, and 2.5-fold higher, respectively, in the uncontrolled NIDDM group than normals. Platelet aggregation in response to ADP (0.25 microM), epinephrine (1.25 microM), and arachidonic acid (0.25 mM) was significantly higher in uncontrolled NIDDM than in normals (75%, 40% and 52%, respectively). Platelet fluorescence polarization was also higher in NIDDM patients indicating decreased membrane fluidity in such patients as compared to normals. After control of blood sugar in 11 NIDDM patients, agonist-stimulated platelet aggregation and other biochemical parameters were comparable to normals.
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PMID:Altered platelet functions in non-insulin-dependent diabetes mellitus (NIDDM). 790 93

The aim of our research was elucidation of a relationship between red cell membrane lipid peroxidation (LPO) and antioxidant defense enzymes, on the one hand, and the age, disease duration, and presence of vascular complications in patients with type I diabetes mellitus, on the other. The possibility of correcting red cell peroxide status with human insulin preparations was investigated. Red cell membrane LPO was found increased more than twofold and antioxidant defense enzymes activities virtually unchanged vs. controls in 16 patients with diabetes aged 20 to 43. These characteristics of red cell peroxidation status do not depend on patients' age, disease standing, or presence of vascular complications. A twelve-week therapy with biosynthetic insulin resulted in complete normalization of LPO processes in patients with angiopathies aged under 35 and with disease standing of less than 10 years. In diabetics with angiopathies aged over 35 and disease standing of more than 10 years red cell MDA level reduced under the effect of therapy with human insulin preparations but was still increased vs. that in healthy donors by 1.5 times. Red cell GP and SOD activities reduced in the course of insulin therapy in all the examined groups of diabetics. Catalase activity increased by approximately 50% in patients with angiopathies, those aged over 35, and a disease standing of more than 10 years under the effect of insulin. In the rest groups of patients catalase activity did not differ from its initial level. Our results permit us recommending besides human insulin preparations antioxidant therapy for patients with vascular complications, those aged over 35, and a disease standing of more than 10 years.
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PMID:[Effect of biosynthetic insulin on lipid peroxidation in erythrocyte membranes in patients with type I diabetes mellitus]. 807 92

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.
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PMID:High dosage vitamin E effect on oxidative status and serum lipids distribution in streptozotocin-induced diabetic rats. 812 91


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