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)

The influence of acute diabetes (8 days), induced by streptozotocin (45 mg.kg-1 body weight) on myocardial and renal antioxidative conditions was investigated. The animals were given subtherapeutical doses of insulin (Interdep 6 U. kg-1 body weight, s.c.). Considerably increased levels of malondialdehyde (MDA), as well as of superoxide dismutase (SOD) and catalase (CAT) activity were found in the myocardium of diabetic animals. The oxidized glutathione (GSSG) level and glutathione peroxidase (GSH-PX) activity remained unchanged. The reduced glutathione (GSH) level as well as the activity of glutathione S-transferase (GST) were significantly lower. The activity of GSH-PX in the kidneys of diabetic rats increased by 60% and that of GST by 105%, respectively. CAT and SOD activity values were unchanged.
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PMID:Antioxidative state of the myocardium and kidneys in acute diabetic rats. 828 Jul 23

The erythrocytes from control (C), diabetic (D) and insulin-treated diabetic (D+I) rats were separated into three ageing groups (TAG) i.e., light dense (young cells), intermediate-dense (middle-aged cells) and heavy-dense (old aged cells) samples. The activities of enzymes and metabolites changed from young to old cells in the following manner: (1) Increase of CAT in TAG and a lower level in D and D+I (2) Decrease of GPx in TAG but a low level in D (3) Increase of GR in TAG but a higher level in D, (4) Increase of GST in C and a decrease in D with a higher level in young cells and a lower level in middle-aged and old cells. The reversal of enzyme was more in young cells of D+I (5) Increase of GSH in TAG, a low level in D and a high level in D+I (6) Increase of GSSG in TAG, a high level found only in young cells of D. The results show that young red cells are affected more significantly in diabetes than other age cell types.
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PMID:Ageing erythrocytes and alloxan diabetes: I. A possible role of catalase, GSH, GSSG, and GSH-enzymes in decreasing defence system. 829 96

Lithium is widely used for treatment of behavioral disorders and has been shown to possess insulin-mimetic properties. The present study examines the in vivo effects of lithium alone, as well as in combination with vanadate (a potent insulin-mimetic agent), on the altered antioxidant status in the liver and kidney of diabetic rats. The elevated blood glucose levels in diabetic rats were about 50% restored by oral administration of lithium (0.3 mg/ml) and were completely normalized following vanadate addition (0.05 mg/ml) to lithium. Lithium therapy effectively normalized the decreased activities of catalase (CAT) and glutathione peroxidase (GSH-PX) but could not restore the lowered superoxide dismutase (SOD) in the liver of diabetic rats; while in kidney, the treatment proved to be ineffective. Inclusion of vanadate produced synergistic effect and caused partial restoration of the altered CAT, GSH-PX and CuZn-SOD levels in diabetic kidney and the depressed SOD activity in diabetic liver. These results suggest that lithium therapy may prove effective in improving the impaired antioxidant status during diabetes and vanadate supplementation at a low dose potentiates the effectiveness of lithium action.
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PMID:Insulin like effects of lithium and vanadate on the altered antioxidant status of diabetic rats. 835 10

The effect of alloxan-induced diabetes on glutathione peroxidase (GSH-Px) activity in sciatic nerve of mice has been studied. We have found, 7 days after alloxan treatment, a significant decrease in this enzymatic activity in the cytosol of sciatic nerve of diabetic mice, and moreover, that these changes remained unaltered up to 21 days after alloxan injection. No modification in the glutathione content of sciatic nerve of diabetic mice was observed throughout the experiment when compared with controls. The decrease in GSH-Px activity in this tissue shows a good correlation with the increase of blood glucose levels throughout the experiment. It is hypothesized whether a combination of mechanisms could be involved in this decrease of GSH-Px activity and if oxygen radicals might be the common mediators of these processes.
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PMID:Decreased glutathione peroxidase activity in sciatic nerve of alloxan-induced diabetic mice and its correlation with blood glucose levels. 839 37

In vivo effects of vanadate on the antioxidant status of control and alloxan diabetic rats liver were examined. The increased oxidative stress during diabetes caused a decline in the activities of glutathione peroxidase (GPx), catalase (CAT), CuZn superoxide dismutase (CuZn-SOD) and Mn-superoxide dismutase (Mn-SOD) in the liver. Reduced glutathione (GSH) was also depleted, but the level of oxidized glutathione and glutathione reductase activity remained unchanged in the livers of diabetic rats. Vanadate treatment of diabetic rats (0.6 mg/mL in drinking water) resulted in almost complete restoration of GPx and Mn-SOD but caused only a partial restoration of CuZn-SOD. However, CAT and GSH were found to be lowered further in vanadate-treated diabetic rats as compared to untreated diabetic rat. Similar decreases in CAT and GSH levels were also observed in the vanadate-treated controls. These results suggest that vanadate, an insulin-mimetic agent, effectively normalized hyperglycemia, but unlike insulin, could not completely restore the altered endogenous defence mechanisms in diabetic liver.
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PMID:Impaired antioxidant status in diabetic rat liver. Effect of vanadate. 844 52

We hypothesized that oxygen free radicals (OFRs) may be involved in pathogenesis of diabetic complications. We therefore investigated the levels of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) and activity of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)] in tissues and blood of streptozotocin (STZ)-induced diabetic rats. The animals were divided into two groups: control and diabetic. After 10 weeks (wks) of diabetes the animals were sacrificed and liver, heart, pancreas, kidney and blood were collected for measurement of various biochemical parameters. Diabetes was associated with a significant increase in TBARS in pancreas, heart and blood. The activity of CAT increased in liver, heart and blood but decreased in kidney. GSH-Px activity increased in pancreas and kidney while SOD activity increased in liver, heart and pancreas. Our findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.
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PMID:Lipid peroxidation and activity of antioxidant enzymes in diabetic rats. 856 56

To elucidate the pathological metabolism of glutathione synthesis in diabetic endothelial cells, we studied the expression of gamma-glutamylcysteine synthetase (gamma-GCS) using a mouse vascular endothelial cell line. Exposing normoglycemic endothelial cells to tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta) increased the activity and the mRNA expression of gamma-GCS. The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. A shift of the concentration of glucose in the medium from 5.5 to 28 mM glucose and a following incubation for 7 days decreased the expression of gamma-GCS mRNA. These cells showed no apparent responses of gamma-GCS mRNA or the activity of NF-kappaB to TNF-alpha or IL-beta. Increase in the GSH concentration of the cells treated with 28 mM glucose restored the expression of gamma-GCS mRNA and its response to TNF-alpha or IL-beta, suggesting that redox regulation is involved in the expression of gamma-GCS. In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus.
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PMID:Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. 866 65

Recently there has been growing interest in magnesium deficiency and its correlation with coronary artery disease, chronic complications of diabetes mellitus and antioxidant enzyme activity. Hypomagnesemia is a common association of diabetes mellitus, and the blood glutathione (GSH) level is significantly lower in both conditions. Metformin (Met), 'an oral antihyperglycemic drug' frequently used in the management of diabetes mellitus outside the USA, has been shown to have an insulin-like action. The purpose of this study was to investigate the effect of oral administration of Met (60 mg kg(-1)) for 14 days on GSH and magnesium levels in blood, liver and heart of normal and streptozotocin-induced diabetic Wistar rats. Diabetes was induced by an i.p. injection of streptozotocin (60 mg kg(-1)). Our results showed that Met did not affect fasting serum glucose concentration in non-diabetic animals but reduced it significantly in diabetic animals. Serum and liver magnesium levels were significantly decreased in the untreated diabetic group compared with the normal group. Treatment with Met improved liver magnesium concentration in the diabetic group only. It has no effect on serum magnesium in diabetic or non-diabetic rats. Heart magnesium levels showed non-significant changes in all groups. In diabetic animals a significant decrease of GSH in both blood and liver was observed. Treatment with Met increased these levels significantly, with a similar effect on GSH levels in non-diabetic rats. There were no significant changes in heart GSH levels in any of the groups. This study demonstrates that oral Met therapy improves the altered levels of magnesium and GSH in diabetic rats.
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PMID:Effect of metformin on glutathione and magnesium in normal and streptozotocin-induced diabetic rats. 866 22

The mechanism involved in diabetes-induced embryotoxicity is still unclear. Mitochondrial alterations probably produced by oxidative stress have been described in embryos developing in a diabetic environment. Furthermore, oxygen radicals-scavenging enzymes can reduce the embryotoxic effects induced by diabetic conditions. In this work we tried to test if glutathione (GSH), a tripeptide implicated in cellular protection against reactive oxygen species, is involved in diabetes-related embryotoxicity. Rat embryos were explanted on day 11 on gestation from normal and from streptozotocin-diabetic mothers. The embryos were examined morphologically, then protein, DNA and GSH were determined both in embryos and in their visceral yolk sacs. The embryos explanted from diabetic mothers showed signs of developmental retardation and 16% were morphologically abnormal. GSH content was reduced in these embryos in comparison to control, but the GSH/protein in the visceral yolk sacs of conceptuses explanted from diabetic mothers was higher than in control visceral yolk sacs. Our hypothesis is that the reduction of embryonic GSH is a consequence of the alteration in GSH transport across the yolk sac endodermal cells damaged by diabetic conditions. The observed reduction in embryonic GSH could reduce the protection against the oxidative stress condition described in diabetic pathology.
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PMID:Glutathione status in diabetes-induced embryopathies. 879 Sep 7

A total of 105 subjects with impaired glucose tolerance were classified into two groups, 51 subjects with plasma glucose > 11.1 mmol l-1 in one of the blood samplings during OGTT, but at 2 h being less than < 11.1 mmol l-1 were classified as early hyperglycaemics. Fifty-four cases were classified as true IGT, with fasting plasma glucose < 7.8 mmol l-1 and post plasma glucose level between 7.8 and 11.1 mmol l-1. Age and sex matched groups of normals (healthy adults) and NIDDM cases without symptomatic secondary complications were also included in the study. Lipid peroxidation (LPO) product in plasma, erythrocyte, and erythrocyte cell membrane were found to be significantly elevated (p < 0.001) in IGT, early hyperglycaemia and diabetes mellitus while glycosylated haemoglobin was also higher. Antioxidant enzymes superoxide dismutase and catalase were significantly lower in red blood cells obtained from IGT and early hyperglycaemic groups. They were closer to the levels showed in NIDDM confirming that antioxidant deficiency is already present in subjects classified as impaired glucose tolerant. Among the antioxidant scavengers, reduced glutathione (GSH) and ascorbic acid are reduced by 15% and 20% in IGT and NIDDM, respectively. We conclude that antioxidant status is poor in both IGT and NIDDM, suggesting an overlap of frank diabetic state in those classified as IGT. It is possible that antioxidant therapy might retard progression from IGT to NIDDM.
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PMID:Abnormal antioxidant status in impaired glucose tolerance and non-insulin-dependent diabetes mellitus. 886 45


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