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

An increased lipid peroxidation, due to the altered intracellular ratio between free radicals and antioxidant systems, has been recently related to diabetes. To study the possible relationship between lipid peroxidation and metabolic control, we measured the plasma concentrations of malondialdehyde (MDA), end product of the oxidation of polyunsaturated fatty acids, in poorly and well controlled Type 2 diabetic patients. A significant increase in plasma malondialdehyde concentrations was found in poorly controlled diabetics when compared to well controlled patients (p < 0.001) and to healthy normoglycaemic subjects (p < 0.001), whereas no significant difference was observed between the two latter groups. Plasma MDA/Cholesterol and MDA/triglyceride ratios were both higher in poorly controlled diabetics than in well controlled (p < 0.005) and in normal subjects (p < 0.01 and p < 0.02 for MDA/CHOL and MDA/TG respectively). In diabetic patients a positive correlation was found between plasma MDA levels and mean daily blood glucose (p < 0.01), plasma fructosamines (p < 0.001), HbA1 (p < 0.05) and plasma triglycerides (p < 0.05), while no significant correlation was shown between plasma malondialdehyde and total cholesterol. Malondialdehyde levels were followed-up for 7 days running (T1-T7) in five poorly controlled diabetics, treated with conventional insulin therapy. This group showed normalized plasma lipid peroxide values (0.486 +/- 0.13 mumol/l, T5, M +/- SEM) 72 h after the restoration of glycaemic control (145 +/- 25 mg/dl, T2, M +/- SEM). These results confirm the increase of lipid peroxidation during Type 2 diabetes. The correlation with the degree of metabolic imbalance suggests a possible role for lipid peroxidation in the occurrence of glucose-induced macromolecular changes.
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PMID:Increased lipid peroxidation in type 2 poorly controlled diabetic patients. 145 13

Malondialdehyde (MDA), a product of lipid peroxidation, was measured in the lens of rats in which diabetes had been induced by treatment with streptozotocin (85 mg/kg). The MDA level increases nearly 100% in lenses from diabetic rats, compared with lenses from age-matched control rats. Treating rats with insulin decreases the MDA content of the diabetic rat lens to normal levels. This suggests that the increase in MDA of diabetic rats lens is not due to a toxic effect of streptozotocin, but instead is the result of diabetes mellitus or insulin deficiency. Administration of the aldose reductase inhibitor, sorbinil, decreases lens MDA levels in diabetic rats in a dose-dependent manner with a median effective dose (ED50) of 7.5 mg/kg. This study demonstrates that sorbinil can prevent lipid peroxidation of rat lens resulting from insulin deficiency, which can aid in helping the lens to cope with the oxidative stress of diabetes.
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PMID:The increase in lipid peroxidation in diabetic rat lens can be reversed by oral sorbinil. 211 76

This study investigated the effect of anisodamine (2 and 5 mg/kg i.v.) on ocular and systemic blood flow distribution in awake lambs using the radioactive microsphere technique. In separate in vitro studies, the effects of anisodamine (at final concentrations of 0.01 to 2.5 mg/ml) were determined on arachidonic acid, alloxan and ultraviolet radiation-induced lipid peroxidation of isolated retinal cells from rabbits and on alloxan-induced lipid peroxidation of hamster pancreatic islet beta cells. Malondialdehyde production was used as an index of lipid peroxidation and measured by the thiobarbituric acid method. Anisodamine preferentially increased blood flow and oxygen delivery to the retina-choroid and iris-ciliary body of the eye by 50-100%. Anisodamine significantly attenuated lipid peroxidation in retinal cells induced by ultraviolet radiation, alloxan and arachidonic acid by 17-50% and protected pancreatic beta cells against alloxan-induced lipid peroxidation. These properties may, in part, account for the beneficial effect of anisodamine in certain patients with diabetes.
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PMID:Anisodamine increases blood flow to the retina-choroid and protects retinal and pancreatic cells against lipid peroxidation. 212 54

There is direct evidence that there is an increase of concentration of oxidizing species and oxidized products in plasma of human diabetics. The extent of this increase seems to reflect a predilection to diabetic damage. 1. A high concentration of lipid hydroperoxide in plasma was observed in diabetic patients and it's levels correlated well with the degree of diabetic nephropathy. 2. Lipid peroxide causes membrane injury of endothelial cells. The addition of anti-oxidant inhibited cell injury markedly. 3. Malondialdehyde and protein (lysin-residual or low density lipoprotein) made conjugates to change the antigenicity. This results shows the possibility that atherosclerosis as diabetic complication may be caused by immunological reactions with modified proteins for example, oxidized LDL and so on. 4. SOD activity in erythrocytes of diabetic patient was extremely decreased compared with non diabetics, but no difference was observed by the ELISA method with monoclonal antibody. Glycosylation had been expected to occur in various kinds of proteins. The inactivation of SOD may be caused by non enzymatic glycosylation, because negative correlation was observed between the activity of SOD and GHb in erythrocytes. This inactivation of SOD may play an important role in the pathogenesis of diabetic complications. From these results, it was suggested that both free radical reactions and non enzymatic glycosylation may play important roles not only in the development of diabetes but also in its complications.
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PMID:[Free radicals and diabetes mellitus]. 220 Sep 13

The purpose of this study was to investigate the roles of decreased synthesis and increased consumption in the depression of arachidonic acid levels in renal cortex and glomeruli of rats with streptozotocin-induced diabetes mellitus. In diabetic rats, arachidonic acid was depressed 33.2% in renal cortex, 47.4% in liver and 66.1% in heart compared to values of control rats. delta 6 Desaturase activity was depressed in renal cortex, liver and heart of diabetic rats to 53.3, 55.5 and 63.7%, respectively, of control values. delta 5 Desaturase activity was also depressed 43.7, 55.5 and 47.6% in renal cortex, liver and heart of diabetic rats, respectively. In other rats the activities of five enzymes involved in the synthesis and esterification of arachidonic acid were measured in renal cortex and in isolated glomeruli. Both tissues from diabetic rats showed depressed activities of delta 5 and delta 6 desaturases, increased activities of long-chain acyl-CoA synthetase and 1-acyl-sn-glycero-3-phosphocholine acyltransferase and no change in the activity of elongase as compared to those in control tissues. Malondialdehyde, an end product of lipid peroxidation, was lower in the renal cortex of diabetic rats than in control rats, whereas beta-oxidation of linoleic acid and arachidonic acid were similar in diabetic and in control rats. Basal and stimulated prostaglandin E2 synthesis were significantly higher in isolated glomeruli from diabetic rats compared to those in control rats. In isolated tubules, prostaglandin E2 synthesis was similarly low in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of decreased arachidonic acid in the renal cortex of rats with diabetes mellitus. 831 52

Malondialdehyde, a marker of lipid peroxidation, was measured as thiobarbituric acid reactive substances (TBARS) in 117 diabetic patients and 53 controls. Patients were divided into groups and subgroups according to the type of diabetes (type 1 and type 2) and the existence or not of vascular complication (macro- or micro-angiopathy). Results showed that TBARS concentrations were significantly higher in type 1 (P < 0.0001) and type 2 (P < 0.001) diabetic patients than in the control group. The plasma TBARS concentrations in type 1 and type 2 diabetic patients did not differ significantly. Among the patients with vascular disease, type 2 diabetic patients with macroangiopathy had significantly higher TBARS concentrations than patients with no vascular complication (P < 0.05). Whichever the type of diabetes, there was no correlation between TBARS concentrations and glycaemic control: glycosylated haemoglobin, fasting blood glucose. This study confirmed the existence of lipid peroxidation disorders in diabetic patients.
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PMID:Plasma malondialdehyde in type 1 and type 2 diabetic patients. 847 88

Intact lenses from New Zealand white rabbits were incubated in tissue culture media containing either 5 mM glucose or 5 mM glucose plus 30 mM galactose. The standard media did not contain taurine. Lenses were also cultured in a third medium containing 30 mM galactose plus 0.2 mM taurine. The frequency of cataract formation was evaluated as a function of the culture media. One lens (1/10), in media containing 5 mM glucose, developed a lenticular opacification during a 72-h incubation. Lenses (12/15) incubated in 30 mM galactose, without taurine, developed cataracts; fewer lenses (2/13) exposed to 30 mM galactose plus 0.2 mM taurine developed cataracts (p < 0.005). Galactose cataracts have been associated with lens edema attributed to the osmotic stress of tissue polyol (galactitol) accumulation. The water content of the noncataractous and cataractous lenses in this experiment did not differ. Lens edema, therefore, was not thought to be important in cataract pathogenesis. Taurine, an organic osmolyte was lower (5.1 +/- 1.5 mumol/g protein) in cataractous lenses than in control lenses (10.0 +/- 1.0 mumol/g protein). Malondialdehyde, an indicator of lipid peroxidation, was higher (36.6 +/- 5.0 mumol/g protein) in lens-containing opacifications than in noncataractous lenses (10.1 +/- 1.9 mumol/gm protein) (p < 0.01). The levels of malondialdehyde suggest that lipid peroxidation was increased in the process of sugar cataractogenesis. The malondialdehyde content of all the lenses correlated inversely (r = -0.53, p < 0.01) with the coincident lens taurine levels. Taurine appears to protect the lens against the development of sugar cataracts; its inverse relationship with lens malondialdehyde suggests this is an antioxidant effect.
J Diabetes Complications
PMID:Taurine prevents galactose-induced cataracts. 848 50

Malondialdehyde, a marker of lipid peroxidation, was measured as thiobarbituric acid-reactive substance in 78 non-insulin-dependent diabetic patients and 28 healthy subjects. Patients were divided into groups and subgroups according to the presence of microalbuminuria and other complications. Plasma and urine malondialdehyde concentrations were significantly higher in patients with and without microalbuminuria than in controls. In contrast to urine malondialdehyde, plasma malondialdehyde levels were significantly higher in microalbuminuric diabetes than in the normolbuminuric diabetic group. There was no correlation between malondialdehyde concentration and glycemic control. This study confirmed the existence of lipid peroxidation disorders in diabetic patients.
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PMID:Plasma and urine malondialdehyde levels in non-insulin-dependent diabetic patients with and without microalbuminuria. 856 81

The objective of the work was to evaluate the effect of short-term hospitalization on metabolic compensation in type 1 diabetics with an intensified insulin regime who are admitted to hospital with the main purpose to participate in an intense educational and therapeutic programme. Twenty patients were examined, mean age 26.3 +/- 6.5 years, mean duration of diabetes 13.2 +/- 8.0 years, who participated in a 5-day educational therapeutic programme which takes place in the authors' department. The level of metabolic compensation was evaluated at the onset and at the end of the hospitalization by means of fructosamine (F), mean blood sugar level, Michaelis index, MAGE (mean amplitude glycaemic excursion), the M value, MDD. During hospitalization in the whole evaluated group an average 6% drop of F was recorded. In the sub-group of patients with a baseline F > 2.6 mmol/l a statistically significant decline occurred from 2.91 +/- 0.14 mmol/l to 2.44 +/- 0.31 mmol/l (p < 0.05). The changes of different indexes calculated from the whole group did not reach statistical significance. In the sub-group with a poorer compensation (F > 2.6 mmol/l), however, the mean blood sugar level declined from 13.48 +/- 2.45 mmol/l to 9.17 +/- 2.05 mmol/l (p < 0.05) and the M value improved from 141.4 +/- 56.6 to 60.5 +/- 40.7 (p < 0.05). The MAGE index deterioration significantly during hospitalization only in the sub-group with a baseline F < 2.6 mmol/l from 2.70 +/- 1.11 to 3.65 +/- 1.28 (p < 0.05). The results indicate that in patients with type 1 diabetes mellitus short-term hospitalization with an educational therapeutic programme need not be associated with a deteriorated metabolic compensation. In those whose compensation is unsatisfactory marked improvement is recorded.
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PMID:[Short-term hospitalization for patient education--effect on metabolic compensation in type I diabetics]. 862 52

Malondialdehyde is a major oxidation product of lipids which is capable of cross-linking the collagen of the cardiovascular system. Identification of cross-links usually involves degradative procedures. In this paper, we use a novel, direct, approach using nuclear magnetic resonance to identify early and labile products. Initial model studies show that malondialdehyde reacts with lysine to form a dihydropyridine derivative rather than the unstable imidopropene Schiff base previously reported. The aldehydes on the pyridine ring could react further to cross-link collagen and stiffen the aorta, thereby promoting further glycation, a process that would be accelerated in diabetes.
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PMID:Formation of a dihydropyridine derivative as a potential cross-link derived from malondialdehyde in physiological systems. 946 2


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