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

Silymarin is a free-radical scavenger and a membrane stabilizer which prevents lipoperoxidation and its associated cell damage in some experimental models. It has been proposed that lipid peroxidation caused by free radicals may be involved in alloxan-induced diabetes mellitus. Alloxan elicits pancreatic lipid peroxidation which precedes the appearance of hyperglycemia in mice. We studied the effects of silymarin on rat pancreas, the effect of this flavonoid on pancreatic, hepatic and blood glutathione (GSH) together with the pancreatic malondialdehyde concentrations in response to alloxan. On its own, silymarin increases pancreatic and blood GSH without changes in either hepatic GSH or in blood glucose. Silymarin prevents the increase in lipid peroxidation produced by alloxan. It also blunts the sustained increment in plasma glucose induced by alloxan. We suggest that silymarin has a protective effect on the pancreatic damage in experimental diabetes mellitus. This may be related to its antioxidative properties and to the increase in concentrations of plasma and pancreatic glutathione.
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PMID:Prevention of alloxan-induced diabetes mellitus in the rat by silymarin. 966 80

Syzigium cumini, commonly known as 'jamun', is widely used in Indian folk medicine for the treatment of diabetes mellitus. Oral administration of 2.5 and 5.0 g/kg body weight of the aqueous extract of the seed for 6 weeks resulted in a significant reduction in blood glucose and an increase in total haemoglobin, but in the case of 7.5 g/kg body weight the effect was not significant. It also prevents decrease in body weight. The aqueous extract also resulted in decreased free radical formation in tissues studied. Thus the study shows that Jamun seed extract (JSEt) has hypoglycaemic action. The decrease in thiobarbituric acid reactive substances (TBARS) and increase in reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) clearly show the antioxidant property of the JSEt. The effect of JSEt was most prominently seen in the case of animals given 5.0 g/kg body weight. JSEt was more effective than glibenclamide.
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PMID:Hypoglycaemic activity of Syzigium cumini seeds: effect on lipid peroxidation in alloxan diabetic rats. 968 76

IDDM results from the destruction of pancreatic beta-cells by autoreactive T-cells that appear to avoid deletion early in development, possibly due to improper interaction with antigen-presenting cells (APCs) resident in the thymus or periphery. In the nonobese diabetic (NOD) mouse, there exists a defect in APC function characterized by its failure to fully mature upon stimulation. The NOD mouse thus provides an excellent model for the investigation of APC dysfunction and development and how these relate to the incidence of autoimmune diabetes. We initiated studies of APC function in the NOD mouse with respect to antigen processing and presentation, using a well-characterized antigen hen egg lysozyme (HEL) and comparing it with the closely related, major histocompatibility complex (MHC) (I-Ag7) identical, diabetes-resistant mouse strain NOR. Proliferation assays comparing NOD and NOR HEL-specific T-cells demonstrated that the T-cell proliferation response of the NOD mouse to both native and denatured forms of the antigen is lower than that of NOR. When crisscross proliferation experiments were conducted using purified T-cells and irradiated spleen cells as APCs from both strains, the results demonstrated that the defect in proliferation resided in the APC compartment of activation. The levels of intracellular glutathione (GSH) were compared in splenic macrophages from NOD and NOR mice; it was found that on antigenic stimulation, NOR macrophages produced significantly more intracellular GSH than did NOD macrophages, even under hyperglycemic (50 mmol/l glucose) conditions. The lower amount of GSH seen in the NOD may result in less efficient processing of antigen, and subsequently, lower levels of T-cell activation.
Diabetes 1998 Aug
PMID:Splenic macrophages from the NOD mouse are defective in the ability to present antigen. 970 19

In our present work we attempt to clarify the pro-, antioxidant status (redox status) of blood and the red blood cell (RBC) filtration changes in type 1 (insulin dependent diabetes mellitus = IDDM) diabetic patients, broadening our biochemical knowledge about the mechanism of disease. Further on we try to apply our observations in therapy. Our studies on enzymes and the pro- and antioxidant status in type 1 diabetes are closely related to earlier works. Our studies on antioxidants have been extended deeper on redox conditions for example on the reduced and oxidized glutathione (GSH and GSSG) and glutathione reductase activity. The properties and changes of antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and catalase) as well as lipid peroxidation (LP) have been studied earlier without selecting the different type of human diabetics. At the same time the red blood cell filtration characteristics are compared also with normal values. The results of our studies confirmed the earlier findings that human diabetes is accompanied by a strong oxidative predominance (oxidative stress) in blood.
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PMID:Pro-, antioxidant and filtration changes in the blood of type 1 diabetic patients. 970 3

This study was conducted on type 2 non-insulin-dependent diabetes mellitus (NIDDM) cases and healthy blood donors. Lipid peroxidation (LP) products in plasma and red blood cell (RBC) hemolysates were estimated as total thiobarbituric acid reactive substances (TTBARS). The plasma and hemolysate reduced and oxidized glutathione (GSH and GSSG) levels are compared. In the hemolysates the antioxidant enzymes namely superoxide dismutase (SOD), glutathione peroxidase (GPx-ase), glutathione reductase (GR-ase) and catalase (C-ase) are also compared. The RBC filtration characteristics are determined and compared with controls: 1. LP and GSH in diabetic plasma were significantly higher, but in the hemolysate the GSH raised but the LP was significantly lower in diabetics than in healthy controls. 2. Superoxide dismutase and C-ase were significantly higher in NIDDM hemolysate. Contrary the GPx-ase activity was significantly lower in diabetics. 3. The diabetic RBCs filtration characteristics are changed in respects significantly namely the Fi was lower, the Tc and CR were higher. It means higher rigidity and oxidative damage of the membrane of diabetic RBCs.
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PMID:Pro-, antioxidant and rheologic studies in the blood of type 2 diabetic patients. 970 4

To evaluate the relationship between oxidative stress and glucose metabolism, insulin sensitivity and intraerythrocytic reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio were measured in 10 non-insulin-dependent diabetes mellitus (NIDDM) patients and 10 healthy subjects before and after the intravenous administration of GSH. In particular, after baseline insulin sensitivity was assessed by a 2-hour euglycemic hyperinsulinemic clamp, either glutathione (1.35 g x m2 x min(-1)) or placebo (saline) were infused over a period of 1 hour. The same protocol was repeated at a 1-week interval, in cross-over, according to a randomized, single-blind design. In healthy subjects, baseline intraerythrocytic GSH/GSSG ratio (P < .0005) and total glucose uptake (P < .005) were significantly higher than in NIDDM patients. In the same subjects, GSH infusion significantly increased total glucose uptake (from 37.1 +/- 6.7 micromol kg(-1) x min(-1) to 39.5 +/- 7.7 micromol x kg(-1) x min(-1), P < .05), whereas saline infusion was completely ineffective. In addition, the mean intraerythrocytic GSH/GSSG ratio significantly increased after GSH infusion (from 21.0 +/- 0.9 to 24.7 +/- 1.3, P < .05). Similar findings were found in diabetic patients, in whom GSH infusion significantly increased both total glucose uptake (from 25.3 +/- 9.0 micromol x kg(-1) x min(-1) to 31.4 +/- 10.0 micromol x kg(-1) x min(-1), P < .001) and intraerythrocytic GSH/GSSG ratio (from 14.8 +/- 4.1 to 21.7 +/- 6.7, P < .01). Pooling diabetic patients and controls, significant correlations were found between intraerythrocytic GSH/GSSG ratio and total glucose uptake (r = .425, P < .05), as well as between increments of the same variables after GSH infusion (r = .518, P < .05). In conclusion, our data support the hypothesis that abnormal intracellular GSH redox status plays an important role in reducing insulin sensitivity in NIDDM patients. Accordingly, intravenous GSH infusion significantly increased both intraerythrocytic GSH/GSSG ratio and total glucose uptake in the same patients.
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PMID:Influence of reduced glutathione infusion on glucose metabolism in patients with non-insulin-dependent diabetes mellitus. 971 98

In this study we investigated the reaction of cyclamate and its major metabolite, cyclohexylamine (CyhNH2), with NaOCl. NaOCl at 100 microM was allowed to react with various concentrations of cyclamate and CyhNH2, and the reactivity was compared with those of reduced glutathione (GSH) and ascorbic acid. The results showed that CyhNH2 was less reactive with NaOCl than GSH but was slightly more reactive than ascorbic acid at concentrations below 50 microM. CyhNH2 at 75 and 100 microM did not further decrease NaOCl. Cyclamate was much less reactive than CyhNH2, with only 43% loss in NaOCl at 100 microM cyclamate. When human blood plasma was incubated with 0.75 microM NaOCl, inclusion of CyhNH2 enhanced oxidation of sulfhydryl groups in a concentration-dependent manner, with complete oxidation of SH groups at 7.5 mM CyhNH2. Cyclamate had no effect. This enhancement by CyhNH2 suggests the formation of reactive products from the reaction of CyhNH2 with NaOCl. Absorption spectra demonstrated that reaction of CyhNH2 with NaOCl at pH 7.4 produced N-monochloramine, as evidenced by the appearance of a new peak at 245 nm and by the disappearance of the 292-nm peak of NaOCl. Cyclamate, which contains a sulfamic acid instead of a primary amine, also reacted with NaOCl at pH 7.4, but the reaction was much less pronounced and the product was probably not monochloramine since the peak was at 270 nm rather than at 245 nm. Because cyclamate is an important sweetener in many countries for people with diabetes mellitus, the possibility exists that CyhNH2 may enhance oxidation of important proteins by HOCl/OCl-.
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PMID:Reaction of cyclohexylamine with hypochlorite and enhancement of oxidation of plasma sulfhydryl groups by hypochlorite in vitro. 973 22

We have studied the effect of the administration of two doses of melatonin (melatonin 100 and melatonin 200 microg/kg bw) on diabetes and oxidative stress experimentally induced by the injection of streptozotocin (STZ) in female Wistar rats. STZ was injected as a single dose (60 mg/kg i.p. in buffered citrate solution, pH 4.0) and melatonin (melatonin 100, 100 microg/kg/day i.p.; melatonin 200, 200 microg/kg/day i.p.) beginning 3 days before diabetes induction and continuing until the end of the study (8 weeks). The parameters analysed to evaluate oxidative stress and the diabetic state were a) for oxidative stress, changes of lipoperoxides (i.e., malondialdehyde, MDA) in plasma and erythrocytes and the changes in reduced glutathione (GSH) in erythrocytes and b) for diabetes, changes in glycemia, lipids (triglycerides: TG; total cholesterol: TC; HDL-cholesterol, HDL-c), percentage of glycosylated hemoglobin (Hb%), and plasma fructosamine. The injection of STZ caused significant increases in the levels of glycemia, percentage of glycosylated hemoglobin, fructosamine, cholesterol, triglycerides, and lipoperoxides in plasma and erythrocytes, whereas it decreased the levels of HDL-c and the GSH content in erythrocytes. The melatonin 100 dose reduced significantly all these increases, except the percentage of glycosylated hemoglobin. With regard to the decreases of plasma HDL-c and GSH content in erythrocytes, this melatonin dose returned them to normal levels. The melatonin 200 dose produced similar changes, though the effects were especially noticeable in the decrease of glycemia (55% vs. diabetes), percentage of hemoglobin (P < 0.001 vs diabetes), and fructosamine (31% vs. diabetes). This dose also reversed the decreases of HDL-c and GSH in erythrocytes. Both doses of melatonin caused significant reduction of the percentage of glycosylated hemoglobin in those groups that were non-diabetic. These illustrate the protective effect of melatonin against oxidative stress and the severity of diabetes induced by STZ. In particular, this study confirms two facts: 1) the powerful antioxidant action of this pineal indole and 2) the importance of the severity of oxidative stress to maintain hyperglycemia and protein glycosylation, two pathogenetic cornerstones indicative of diabetic complications. Melatonin reduces remarkably the degree of lipoperoxidation, hyperglycemia, and protein glycosylation, which gives hope to a promising perspective of this product, together with other biological antioxidants, in the treatment of diabetic complications where oxidative stress, either in a high or in a low degree, is present.
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PMID:Oxidative stress in diabetic rats induced by streptozotocin: protective effects of melatonin. 975 30

High resolution B-mode ultrasonography of the carotid arteries has been used to investigate the signs of early atherosclerotic vessel wall disease by measuring the intima-media thickness (IMT). We examined the association between IMT and lipid peroxidation and found IMT to be increased in a group of patients with respect to controls (1.430+/-0.341 mm versus 0.703+/-0.201 mm, P < 0.001). Plasma and erythrocyte malondialdehyde (MDA) levels were also significantly higher (P<0.001) and the erythrocyte reduced glutathione (GSH) levels were significantly lower (P <0.001) in the patients with respect to the controls. In the groups of patients there was no significant correlation between the mean IMT and the plasma and erythrocyte MDA levels or the erythrocyte GSH levels. In conclusion determination of lipid peroxides would be especially important and advisable in patients with increased carotid IMT. Type II diabetes and hypertension were also associated with increased IMT.
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PMID:A study on the carotid artery intima-media thickness and its association with lipid peroxidation. 977 48

Experimental studies carried out in vitro suggest a role of oxidative stress in diabetes-induced embryopathies. Glutathione is the main defense against free radicals in embryonic as it is in adult tissues. In this experiment, using postimplantation whole-embryo culture, we analyze: (1) the effects of serum from streptozotocin-induced diabetic rats on embryonic development and on glutathione distribution between the yolk sac and embryonic tissues and (2) the role of glutathione in preventing embryopathies (using the inhibitor of glutathione synthesis buthionine sulfoximine). Our data show that in rat embryos cultured in diabetic serum, the only observed effects are at the yolk sac level. No effects on the glutathione content were observed. The addition of buthionine sulfoximine reduced the glutathione content and produced signs of developmental delay in embryos cultured in diabetic serum, suggesting a role of the oxidative stress in producing diabetes-related embryotoxicity.
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PMID:Development of rat embryos cultured in serum from diabetic rats. 983 86


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