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)

Alterations in superoxide dismutase activity, observed in erythrocytes of children with insulin-dependent form of diabetes mellitus, depended on the age of patients, severity and degree of the disease compensation. Content of lipid peroxidation products was also dissimilar in compensated and decompensated forms of diabetes mellitus. Activity of catalase in erythrocytes of patients was similar to corresponding values of healthy children and did not depend on the disease stage and severity. Estimation of superoxide dismutase activity and content of diene ketons were most suitable patterns for monitoring treatment of diabetes in children.
 ...
PMID:[Activity of antioxidative enzymes and lipid peroxidation in erythrocytes of children with diabetes mellitus]. 234 73

Eicosanoid metabolism is altered by diabetes. However, postischemic responses of diabetic hearts (DH) to eicosanoids such as prostacyclin are unknown. a prostacyclin analogue iloprost (Ilo) was given to isovolumically beating rat hearts during 20 min of total global ischemia and 30 min of reperfusion. Acute DH (48 h) but not chronic DH (2 mo) had pronounced postischemic dysfunction (developed pressure = 22 +/- 11%), which was completely reversed by 3 X 10(-8) M Ilo (developed pressure = 113 +/- 15%). Ilo also stimulated endogenous prostacyclin release in postischemic control hearts (CH) but not acute or chronic DH. Ilo significantly decreased postischemic recovery in CH (from 67 +/- 11 to 15 +/- 4%), which was partially blocked by the coadministration of the calcium-entry blocker diltiazem or almost completely reversed by the free radical scavengers superoxide dismutase plus catalase (100 U/ml). These data suggest that Ilo may promote functional recovery in DH at concentrations that produce dysfunction in CH. Furthermore, Ilo may induce dysfunction in CH by a calcium ionophoretic action, which appears depressed in diabetes, and by concomitant free radical production (presumably via prostaglandin hydroperoxidases) during Ilo-stimulated endogenous prostacyclin synthesis.
 ...
PMID:Diabetes alters postischemic response to a prostacyclin mimetic. 247 Feb 63

The cellular effects of retinoids may be relevant to protection against chemical-induced diabetes mellitus. To determine whether retinyl palmitate protects the beta cell from streptozotocin- and alloxan-induced diabetes, we injected streptozotocin, 60 mg/kg, or alloxan, 100 mg/kg, with or without varying doses of retinyl palmitate intraperitoneally or by tail vein. Plasma glucose was measured for over 4 weeks. To determine if the protective effects of retinyl palmitate were mediated through effects on superoxide dismutase, a scavenger of tissue free radicals, we determined whether retinyl palmitate affected islet superoxide dismutase activity. Retinyl palmitate, given intraperitoneally or by tail vein, protected against both streptozotocin- and alloxan-induced diabetes. The effect was dependent on the route of administration. When given intraperitoneally, the protective effect was greater than when given intravenously. When given by tail vein, the protective effect was dose dependent. Retinyl palmitate in vitro did not affect insulin secretion or islet superoxide dismutase. We conclude that retinyl palmitate treatment protects against streptozotocin- and alloxan-induced diabetes. Further studies are needed to determine whether retinyl palmitate protects against the development of diabetes in other animal models and whether this effect is relevant to diabetes in man.
 ...
PMID:Protective effects of retinyl palmitate on streptozotocin- and alloxan-induced beta cell toxicity and diabetes in the rat. 252 47

Spontaneous diabetes in the non-obese diabetic (NOD) mice is a CD4 T cell-dependent process. We have suggested that specific beta cell destruction results from free radical production at the site of islet inflammation; oxygen radicals are produced by activated inflammatory cells. We reported here that in vivo treatment of spontaneously diabetic NOD mice with the enzyme superoxide dismutase (2000 U for seven injections) and catalase (40,000 U for seven injections) protects islet tissue from disease recurrence following transplantation into spontaneously diabetic mice. Similar results were obtained when animals were treated with either enzyme alone. This effect was dose-dependent and little protection was observed when the dose of enzyme was reduced four-fold. These results indicate that oxygen metabolites, specially superoxide and hydrogen peroxide, are directly involved in the pathogenesis of immunology mediated diabetes.
 ...
PMID:Involvement of O2 radicals in 'autoimmune' diabetes. 254 56

The effect of short term (2-wk) diabetes induced by streptozotocin and starvation (1-wk) on antioxidant enzymes and lipid peroxidation in the liver, kidney and heart of rats was investigated. The activity of mitochondrial oxidative markers was increased in diabetic liver and kidney, while the activity in tissues of starved rats tended to be decreased. Immunoreactive manganese superoxide dismutase was increased only in diabetic liver and was unchanged or decreased in the rest of the tissues. Glutathione peroxidase activity was increased in tissues of diabetic but not starved rats. The changes in copper-zinc superoxide dismutase and catalase in diabetic rats were similar to those in starved rats. In both groups, copper-zinc superoxide dismutase was decreased in liver, while catalase activity was decreased in liver and kidney, and increased in heart. The lipid peroxide level was increased in diabetic kidney and in the heart of starved rats, and decreased in the rest of the tissues. Insulin treatment in diabetic rats and refeeding in starved rats restored most of the abnormalities toward normal. These results suggest that accelerated mitochondrial oxidative metabolism not accompanied by induction of manganes superoxide dismutase results in oxidative injury in the hypertrophied kidney at an early stage of diabetes and possibly contributes to the development of nephropathy. Peroxidative myocardial damage in starved rat appears to be mediated by a catabolic process.
Diabetes Res 1989 Oct
PMID:Antioxidant enzyme status and lipid peroxidation in various tissues of diabetic and starved rats. 256 53

Diabetic patients with hypertriglyceridemia frequently develop atherosclerosis. Because superoxide (O2-) is suspected to play an important role in the initiation of atherosclerosis, we investigated whether an abnormal amount of O2- was produced by circulating mononuclear cells of patients with both diabetes mellitus and hypertriglyceridemia. The rate of production of superoxide dismutase-inhibitable O2- was measured when cells were stimulated by either 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) or by opsonized zymosan (OZ). In addition, the rates of O2- production by mononuclear cells drawn from three other groups (normal, solely diabetic, and solely hypertriglyceridemic) were determined. We found that the rate of O2- production by mononuclear cells from the diabetic hypertriglyceridemic group was significantly higher than that from normal, diabetic, and hypertriglyceridemic groups. When the rates of O2- production by mononuclear cells were plotted against the levels of plasma triglyceride for all individuals tested, they correlated positively (r = .73 in PMA stimulation and r = .79 in OZ stimulation, P less than .01). However, the rate of O2- production did not relate to other parameters, i.e., plasma cholesterol level, hemoglobin A1 level in erythrocytes, and the molar ratio of free cholesterol to phospholipid in mononuclear cells. Thus, we concluded that the observed elevated rate of O2- production in the diabetic hypertriglyceridemic mononuclear cells was a reflection of a hypertriglyceridemic condition and was not unique to the diabetic hypertriglyceridemic condition. Also, O2- may be involved in the pathogenesis of atherosclerosis in diabetic hypertriglyceridemic patients when atherogenic factors specific to diabetes are concomitantly present.
Diabetes 1988 Jun
PMID:Increased superoxide production by mononuclear cells of patients with hypertriglyceridemia and diabetes. 283 56

Amino sugars such as galactosamine are hepatotoxic. It has been verified that toxic hepatitis induced by galactosamine is similar to that of CCl4 poisoning, and that both were inhibited by O2* scavengers. Fructosamine results from the union of glucose with the epsilon-amine of lysine. A test for fructosamine quantification is based on nitroblue tetrazolium (NBT) reduction, in which O2- is involved, the reduction being inhibited in the presence of superoxide dismutase (SOD). Given these facts, we attempted to elucidate if galactosamine and glucosamine reduce NBT and if that reduction is inhibited by SOD. This was confirmed. Subsequently, we incubated aminoacids (glycine, lysine, alanine) with glucose and galactose for 7 days and studied the action of the incubation products on NBT, using amino acids and sugars as controls. We found that NBT reduction increases proportionally to the length of incubation time of glucose/galactose with lysine, but not with other amino acids. Reduction of NBT by the Amadori compounds formed is inhibited by SOD. We suggest that oxygen radical generation by Amadori compounds must be taken into consideration as one cause of damage in diabetes of long duration.
 ...
PMID:Oxygen radical generation by Maillard compounds. 283 94

Several D-sugars were incubated with L-lysine or with L-arginine for 10 days. The resulting compounds are able to reduce nitrobluetetrazolium (NBT). This is prevented by superoxide dismutase (SOD), indicating that the superoxide radical is generated by the resulting Amadori compounds. The formation of superoxide radical in vivo, as a result of nonenzymatic glycosylation of proteins, may be considered to be a contributory factor to the appearance of chronic complications of diabetes.
 ...
PMID:Superoxide radical generation by Amadori compounds. 285 11

Acetyl-homocysteine-thiolactone (CYT) is an organic thio compound that exerts free radical scavenger activity and increases superoxide dismutase (SOD) activity. Administration of 32 mg CYT/kg body wt/day/30 days in rats increased SOD activity in erythrocytes by 126%, and in pancreatic islets by 202%. Treatment affected only the Cu-Zn fraction of the enzyme. Transmission electron microscope observations showed that the damage to the pancreatic beta cells induced by single or multiple subdiabetogenic doses of streptozocin (STZ) (45 mg/kg body wt) was attenuated in animals treated with CYT. This protective effect was not observed with 65 mg of STZ. The experimental results seem to support the hypothesis that pancreatic beta cells are particularly vulnerable to the effect of oxygen radicals and that the cytotoxic effect of STZ is related to free radical-induced peroxidation.
Diabetes 1986 Apr
PMID:Acetyl-homocysteine-thiolactone-induced increase of superoxide dismutase counteracts the effect of subdiabetogenic doses of streptozocin. 293 74

The potential of nickel chloride to prevent streptozotocin-induced hyperglycemia was tested in rats in vivo. To induce diabetes, streptozotocin (100 mg/kg body weight) was injected as a single dose. Streptozotocin treatment resulted in a significant decrease in plasma insulin and ceruloplasmin, and pancreatic Cu, protein, and Cu-Zn superoxide dismutase activity. In rats treated with nickel chloride (10 mg/kg body weight) and streptozotocin, these values were comparable with those observed in control rats. The results indicate that nickel chloride injected before streptozotocin prevented streptozotocin-induced hyperglycemia, and suggest that the protective effect was related to Cu-Zn superoxide dismutase activity, mediated by copper.
 ...
PMID:Effect of nickel chloride on streptozotocin-induced diabetes in rats. 304 20


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