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

Diabetes mellitus (DM) is a common disease affecting over 124 million individuals worldwide. DM is associated with high risk of atherosclerosis and renal, neural, and ocular damage. Increased oxidant stress has been implicated in the pathogenesis of DM. An increase in serum ceruloplasmin (Cp) levels has also been reported in Type 2 DM. Cp permits the incorporation of iron into transferrin (Trf). Trf inhibits iron ion-dependent OHo formation from H2O2. Patients with diabetes have increased levels of plasma lipid peroxidation products. In this study, we evaluated 50 patients with Type 2 DM and 21 clinically healthy subjects. Patients were divided into two groups. Group I included 29 patients without diabetic complications, Group II 21 with diabetic complications. Serum Cp, Trf, C-reactive protein (CRP), triglyceride (TG), cholesterol (Chol), and malondialdehyde (MDA) levels are studied. Serum Cp, CRP, TG, Chol, and MDA levels in diabetic patients were significantly higher than those of controls. Trf levels were significantly lower in diabetic patients than those of the controls. Cp, CRP, HbA1C, and MDA levels in Group II were significantly higher than those of Group I. Our results indicate that oxygen free radicals are formed in DM and can result in diabetic complications and that a prooxidant/oxidant imbalance is involved in the tissue injury in DM and diabetic complications.
J Diabetes Complications
PMID:Levels of ceruloplasmin, transferrin, and lipid peroxidation in the serum of patients with Type 2 diabetes mellitus. 1520 35

Clinical research has confirmed the efficacy of several plants in the modulation of oxidative stress associated with diabetes mellitus. Scoparia dulcis plant extract is tried for prevention and treatment of diabetes mellitus induced experimentally by streptozotocin injection. A single dose of streptozotocin (45 mg/kg body weight) produced decrease in insulin, hyperglycemia, increased lipid peroxidation (Thiobarbituric reactive substances and lipid hydroperoxides) and decreased antioxidant levels (vitamin C, vitamin E, reduced glutathione, ceruloplasmin). Oral administration of an aqueous extract of Scoparia dulcis plant (200 mg/kg body weight) for 6 weeks to diabetic rats significantly increased the plasma insulin and plasma antioxidants and significantly decreased lipid peroxidation. The effect of Scoparia dulcis plant extract at 200 mg/kg body weight was better than that of glibenclamide, a reference drug.
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PMID:Effect of scoparia dulcis (Sweet Broomweed) plant extract on plasma antioxidants in streptozotocin-induced experimental diabetes in male albino Wistar rats. 1529 95

Increased oxidative stress has been suggested to be involved in the pathogenesis and progression of diabetic tissue damage. The aim of this study was to investigate the effect of ethanolic extract of Eugenia jambolana seed kernel on antioxidant defense systems of plasma and pancreas in streptozotocin-induced diabetes in rats. The levels of glucose, vitamin-C, vitamin-E, ceruloplasmin, reduced glutathione and lipidperoxides were estimated in plasma of control and experimental groups of rats. The levels of lipidperoxides, reduced glutathione and activities of superoxide dismutase, catalase and glutathione peroxidase were assayed in pancreatic tissue of control and experimental groups of rats. A significant increase in the levels of plasma glucose, vitamin-E, ceruloplasmin, lipid peroxides and a concomitant decrease in the levels of vitamin-C, reduced glutathione were observed in diabetic rats. The activities of pancreatic antioxidant enzymes were altered in diabetic rats. These alterations were reverted back to near normal level after the treatment with Eugenia jambolana seed kernel and glibenclamide. Histopathological studies also revealed that the protective effect of Eugenia jambolana seed kernel on pancreatic beta-cells. The present study shows that Eugenia jambolana seed kernel decreased oxidative stress in diabetic rats, which inturn may be due to its hypoglycemic property.
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PMID:Effect of Eugenia Jambolana seed kernel on antioxidant defense system in streptozotocin-induced diabetes in rats. 1536 6

The diabetes mellitus occurs as an important disease at elderly people, to whom the micro- and macrovascular complications represent a major cause of morbidity and mortality. Experimental researches of the last years proved that the oxidative stress may be the common mechanisms that intervenes in the occurrence of the diabetes complications as well as in the aging process and is responsible for the increased prevalence of chronic complications at elderly diabetics. Starting from this information, we performed a comparative study where we followed the intensity of the oxidative stress at elderly diabetics as compared to adult diabetics and non-diabetic elderly people. At the same time, we have followed the involvement of oxidative stress in the occurrence of diabetic microangiopathy and atherosclerosis. 155 patients from the 4th Medical Clinic were studied during 2000-2003. These patients were divided into three lots: lot 1: elderly diabetics, lot 2: adult diabetics, lot 3: elderly non-diabetics. At these patients we have followed comparatively the intensity of the oxidant status by determining the plasma malondialdehyde (MDA) and the anti-oxidant status by determining the plasma ceruloplasmin, as well as the correlations of these two parameters with the chronic complications of diabetes. At elderly diabetics there is an increased oxidative stress underlined by an increased plasma level of MDA and ceruloplasmin as compared to the adult diabetics and non-diabetic elderly people and this increased oxidative stress is involved in the development of the chronic complications at this patients. In case of elderly diabetics, the age and the illness may induce the formation of oxygen-derived free radicals with synergic effect in injuring tissues and organs.
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PMID:The oxidative stress in the development of diabetes chronic complications in the elderly. 1552 29

Aceruloplasminemia is an autosomal recessive disorder of iron metabolism caused by mutations in the ceruloplasmin (Cp) gene. We reported the results of clinical and molecular studies on a Japanese family with aceruloplasminemia. A 58-year-old man who had had diabetes mellitus for more than 30 years developed cerebellar ataxia several years before. He was found to have mild retinal degeneration too. Laboratory findings revealed a complete deficiency of serum ferroxidase activity and undetectable serum Cp. Magnetic resonance imaging showed a pronounced hypointensity in the bilateral putamina, caudate, thalamus and dentate nuclei on both T1- and T2-weighted images suggesting the presence of iron overload. We identified a homozygous deletion mutation (nt2602 delG) of the Cp gene in the patient, and the same heterozygous mutation in his unaffected father. To date, at least 29 mutations in the Cp gene have been identified. Although an individual with a heterozygous mutation has been believed to be an asymptomatic carrier like his father, some patients with such a condition were recently described to show neurological deficits. The variation in clinical findings may be explained partly by the difference in the severity of generation of free radicals caused by iron deposition or the environmental factors such as aging. Further investigations would be required to elucidate the molecular mechanisms of this late onset neurodegeneraion.
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PMID:[A case of aceruloplasminemia presenting as cerebellar ataxia with homozygous mutation nt2602 delG]. 1560 77

The main purpose of this article is to review the previously published data on so-called "moose sickness" in the light of two case studies presented here. Molybdenosis and Mo-induced disturbances of Cu metabolism in moose are characterized by numerous severe lesions caused by reduced activity of Cu-containing enzymes such as ceruloplasmin, superoxide dismutase in blood, and myocardial cytochrome c oxidase. Consequences of such metabolic disturbances (e.g. glucose intolerance, insulin resistance, and non-insulin-dependent diabetes mellitus) were first reported in moose in 2000. This was corroborated by the detection of furosine, pentosidine, and Nepsilon-(carboxymethyl)-lysine in blood plasma and the kidney, indicating long-term hyperglycemia. Increased concentrations of insulin, glucose, and urea and reduced levels of phosphate, T4, and Mg in blood were also seen. Recently, a similar toxic endocrinopathy was reported in sheep treated therapeutically with thiomolybdates because of chronic Cu toxicosis. Two case reports illustrate the difficulty of diagnosing Mo-related disturbances of Cu metabolism in moose, as analyses of Cu and Mo have not proved entirely reliable because of interaction, accumulation, and the short biological half-life of Mo. The increased bioavailability of Mo is most probably the result of increased pH in the soil, caused, for example, by liming, making Mo accessible in forage plants consumed by moose. The etiology underlying the Swedish moose disease has been difficult to determine because of the complex clinical signs and unspecific pathological findings. However, a combination of clinical chemistry, trace element analysis, and biochemistry correlated with the pathological findings has corroborated molybdenosis and Mo-induced disturbances of Cu metabolism as the probable etiological factor. Alternative etiologies suggested for the moose disease, such as viral infection, starvation because of overpopulation, and/or shortage of forage as well as senescence and phytotoxic substances, are discussed.
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PMID:A review of the "mysterious" wasting disease in Swedish moose (Alces alces L.) related to molybdenosis and disturbances in copper metabolism. 1562 35

Cross-sectional studies have reported strong correlations between plasma levels of complement C3, insulin, and glucose. This prospective study explored whether elevated levels of C3, C4, and other inflammation-sensitive plasma proteins (ISPs; fibrinogen, orosomucoid, alpha1-antitrypsin, haptoglobin, and ceruloplasmin) are associated with the development of diabetes. Plasma proteins were measured in 2,815 nondiabetic healthy men, age 38-50 years, who were reexamined after a mean follow-up of 6.1 years. Diabetes development (n = 123) was studied in relation to baseline levels of plasma proteins. After adjusting for age, screening year, and glucose at baseline, the odds ratio (95% CI) for developing diabetes was 1.00, 2.4 (1.1-5.3), 2.9 (1.4-6.0), and 5.6 (2.8-10.9), respectively, for men with C3 in the 1st, 2nd, 3rd, and 4th quartiles (trend: P < 0.00001). Fibrinogen, haptoglobin, C4, and the number of elevated ISPs were also related to future diabetes in this model. Only C3 was significantly associated with diabetes development after further adjustments for potential confounders, including BMI, insulin, and other inflammatory markers. We concluded that the risk of developing diabetes is related to levels of complement C3.
Diabetes 2005 Feb
PMID:Complement C3 is a risk factor for the development of diabetes: a population-based cohort study. 1567 17

Aceruloplasminemia is a rare autosomal recessive disorder. The lack of ceruloplasmin ferroxidase activity leads to parenchymal and reticuloendothelial iron overload, resulting in diabetes and progressive neurodegeneration with extrapyramidal disorders, ataxia, and dementia. We describe the MR imaging findings in a 40-year-old woman with hereditary aceruloplasminemia. The abnormal T2 hypointensities were more marked than those seen in any other condition, including degenerative disorders of the basal ganglia and Wilson disease, and they may be typical of aceruloplasminemia. To our knowledge, involvement of the cortex has not been described and suggests that brain iron accumulation in aceruloplasminemia is more extensive than previously believed, even in asymptomatic patients.
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PMID:MR imaging of cerebral cortical involvement in aceruloplasminemia. 1576 Aug 83

Aminoacetone (AA), a putative endogenous source of cytotoxic methylglyoxal, and ceruloplasmin (CP), the antioxidant plasma copper transporter, are known to increase in diabetes. AA was recently shown in vitro to act as a pro-oxidant toward ferritin and isolated mitochondria. We now report AA oxidative effects on CP mediated by AA-generated reactive oxygen species (ROS). Incubation of 1.5 microM human CP with 0.05-1 mM AA resulted in extensive protein aggregation. That ROS-driven thiol cross-linking underlies the CP aggregation was evidenced by the inhibitory effects of added superoxide dismutase, catalase, mannitol, and dithiothreitol. The addition of CP to AA (mM) solutions accelerated oxygen consumption by AA and caused CP copper ion release and loss of ferroxidase and aminoxidase activities. If operative in vivo, this reaction would impair the antioxidant role of CP and iron uptake by ferritin and hence contribute to intracellular iron-induced oxidative stress during AA accumulation in diabetes mellitus.
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PMID:Aminoacetone induces oxidative modification to human plasma ceruloplasmin. 1583 36

Perturbations in copper (Cu) metabolism are a characteristic of diabetes, for example, elevated plasma Cu and compromised oxidant defense related to diabetes-induced effects on Cu-containing enzymes. Herein, the redistribution of Cu in selected tissues is described in response to diabetic and nondiabetic states in rats that were fed diets adequate in (12 mg Cu/kg of diet) or deficient in (no added Cu) Cu. Diabetes was induced by intravenous administration of streptozotocin (40 mg/kg body weight). After 5 weeks, rats were gavaged with (67)Cu (0.74 MBq per rat) using the Cu-deficient diet as a vehicle (suspended 1:3 in water) and killed at various time points. The use of (67)Cu allowed for the assessment of short-term Cu distribution and its comparison to the steady-state Cu distribution, as determined by direct Cu analysis. In contrast to control rats, the adaptive mechanisms for Cu homeostasis in diabetic rats were impaired. In general, measures of Cu retention were reduced in diabetic rats compared to corresponding values for control rats. Moreover, diabetic rats had low copper, zinc superoxide dismutase activity that was reduced even further when diabetic rats were fed with low-Cu diets. However, liver and kidney metallothionein and plasma ceruloplasmin levels were elevated in diabetic rats compared to control rats. Such diabetes-related metabolic alterations were taken as measures of increased oxidative stress and inflammation, which may have implications in the progression of diabetes-related pathologies.
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PMID:Diabetes and dietary copper alter 67Cu metabolism and oxidant defense in the rat. 1586 32


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