Metabolic Control May Influence the Increased Superoxide Generation in Diabetic Serum

Ceriello, Antonio; Giugliano, Dario; Quatraro, A; Russo, P. Dello; Lefèbvre, Pierre

doi:10.1111/j.1464-5491.1991.tb01647.x

Cited by 106 publications

(60 citation statements)

References 12 publications

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“…In providing support for possible increased rates of glucose autoxidation and the subsequent generation of free radicals, the diabetic group in this study showed higher blood glucose levels, thus providing more substrate for autoxidation purposes. In addition, it has been suggested that poor metabolic control may influence the generation of O 2 · − radicals in diabetic serum [3]. This is partially supported our data demonstrating a higher HbA 1c level in the diabetic group.…”

Section: Discussionsupporting

confidence: 90%

“…Reports suggest that patients with diabetes mellitus are susceptible to increased levels of oxidative stress [1,2], although it is not known whether the increase in reactive oxygen species (ROS) is a causative factor or merely an epiphenomenon. Poor intravascular substrate control is largely regarded as a factor contributing to the increase in superoxide anions (O 2 · − ) that has previously been observed in diabetic serum [3]. Other potential mechanisms relating to enhanced oxidative stress in diabetes include a compromised antioxidant defence system, glucose autoxidation, the formation of advanced glycated end-products and a change in the glutathione redox status [4].…”

Section: Introductionmentioning

confidence: 99%

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Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

et al. 2008

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Aims/hypothesis Patients with type 1 diabetes mellitus are more susceptible than healthy individuals to exercise-induced oxidative stress and vascular endothelial dysfunction, which has important implications for the progression of disease. Thus, in the present study, we designed a randomised doubleblind, placebo-controlled trial to test the original hypothesis that oral prophylaxis with vitamin C attenuates rest and exercise-induced free radical-mediated lipid peroxidation in type 1 diabetes mellitus. Methods All data were collected from hospitalised diabetic patients. The electron paramagnetic resonance spectroscopic detection of spin-trapped α-phenyl-tert-butylnitrone (PBN) adducts was combined with the use of supporting markers of lipid peroxidation and non-enzymatic antioxidants to assess exercise-induced oxidative stress in male patients with type 1 diabetes (HbA 1c 7.9±1%, n=12) and healthy controls (HbA 1c 4.6±0.5%, n=14). Following participant randomisation using numbers in a sealed envelope, venous blood samples were obtained at rest, after a maximal exercise challenge and before and 2 h after oral ingestion of 1 g ascorbate or placebo. Participants and lead investigators were blinded to the administration of either placebo or ascorbate treatments. Primary outcome was the difference in changes in free radicals following ascorbate ingestion. Results Six diabetic patients and seven healthy control participants were randomised to each of the placebo and ascorbate groups. Diabetic patients (n=12) exhibited an elevated concentration of PBN adducts (p<0.05 vs healthy, n=14), which were confirmed as secondary, lipid-derived oxygen-centred alkoxyl (RO·) radicals (a nitrogen =1.37 mT and aβ hydrogen =0.18 mT). Lipid hydroperoxides were also selectively elevated and associated with a depression of retinol and lycopene (p<0.05 vs healthy). Vitamin C supplementation increased plasma vitamin C concentration to a similar degree in both groups (p<0.05 vs presupplementation) and attenuated the exercise-induced oxidative stress response (p<0.05 vs healthy).There were no selective treatment differences between groups in the primary outcome variable. Conclusions/interpretation These findings are the first to suggest that oral vitamin C supplementation provides an Diabetologia

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

et al. 2008

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“…Thus, Amadori albumin can be associated with diabetic nephropathy, and it can be localised in retinal capillaries from diabetic patients [38]. Furthermore, all these studies are also consistent with the idea that oxidative stress observed in patients or diabetic animals is directly related to the metabolic control of the disease [33,34,35,36,37,38,46,47,48].…”

Section: Discussionsupporting

confidence: 71%

Early and intermediate Amadori glycosylation adducts, oxidative stress, and endothelial dysfunction in the streptozotocin-induced diabetic rats vasculature

et al. 2003

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Aims/hypothesis. In a model of streptozotocin-induced Type 1 diabetes mellitus in rats of 9 weeks duration, we analysed time associations between the development of hyperglycaemia, early and intermediate glycosylation Amadori adducts, or AGE compared with enhancement of oxidative stress and endothelial dysfunction.Methods. Endothelial function was tested at several stages of streptozotocin-induced diabetes and after treatment with insulin, resulting in different concentrations of blood glucose, glycosylated haemoglobin (an Amadori adduct), and AGE. Other animals were studied antagonising the formation of AGE with aminoguanidine. Results. Relaxation in response to acetylcholine (1 nmol/l to 10 µmol/l) was tested in isolated segments from aorta or mesenteric microvessels. Impairment of endothelium-dependent relaxations occurred after 2 weeks of untreated diabetes. Preincubation of vessels affected with 100 U/ml superoxide dismutase improved the relaxations to acetylcholine, along the time-course of the endothelial impairment. This indicates the participation of reactive oxygen species on diabetic endothelial dysfunction. The impairment of endothelium-dependent relaxations was recovered after 3 more weeks of insulin treatment. Aminoguanidine treatment did not modify this pattern of development. The time course of the rise and disappearance of endothelial dysfunction showed a higher correlation with glycosylated haemoglobin concentrations than with blood glucose or serum AGE. Conclusion/interpretation. Enhancement of early and intermediate Amadori adducts of protein glycosylation was the factor showing a better relation with the development of endothelium impairment. These results are consistent with a role for these products in the development of diabetic vasculopathy. [Diabetologia (2003) 46:556-566] Keywords Diabetes mellitus, endothelial dysfunction, nitric oxide, superoxide anions, hyperglycaemia, Amadori adducts, advanced glycosylation end-products. Endothelial dysfunction seems to be a key factor in the development of diabetic vascular complications. The impairment of endothelium-dependent vasodilatations is an early event occurring in diabetic patients [1,2,3] and animal diabetic models [4,5,6, 7]. Enhanced oxidative stress in diabetes mellitus has been also shown [8,9], which can be detected by peroxidation products [10] or by increased generation of reactive oxygen species (ROS), mainly superoxide anions [11]. Indeed, enhanced oxidative stress is proposed to be a major cause of diabetic endothelial dysfunction [12,13].There is also increasing evidence that diabetic endothelial dysfunction and oxidative stress are a conse-

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“…Ceriello and cols. (17) were able to demonstrate a significant increase in the production of superoxide anions (SOA) in 10 patients with T1DM, although the study was limited to adult subjects. On the other hand, Hsu and cols.…”

Section: Discussionmentioning

confidence: 98%

Oxidative stress and interleukin-6 secretion during the progression of type 1 diabetes

Reis

Amaral

Volpe

et al. 2012

Arq Bras Endocrinol Metab

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Objective: To evaluate inflammatory, oxidizing, and reducing responses during the progression of type 1 diabetes mellitus (T1DM) in patients without chronic complications. Subjects and methods: Plasma antioxidant status, reactive oxygen species (ROS), and interleukin-6 (IL-6) were measured in 42 patients with T1DM and in 24 healthy subjects. Results: Significant increases were detected in the median values of ROS and IL-6 in patients with T1DM compared with healthy subjects (ROS ~ 4,836 vs. 2,036 RLU/min, respectively; P < .05: IL-6 ~ 14.2 vs. 9.7 pg/mL, respectively; P = .002). No significant between-group differences (P > 0.05) were observed in oxidizing responses or in IL-6 concentrations when diabetic patients were grouped according to time after diagnosis (0 -10, 10 -20 and > 20 years). Plasma antioxidant responses were similar in patients with T1DM and in healthy subjects. Conclusions: Our results demonstrate that oxidizing and inflammatory responses are increased at the onset of T1DM, but remain unchanged during disease progression. These findings suggest that functional changes involved in diabetic complications may commence in the first years after diagnosis. Arq Bras Endocrinol Metab.2012;56(7):441-8 Keywords Type 1 diabetes; disease progression; oxidative stress; plasma antioxidant status RESUMO Objetivo: Avaliar as respostas inflamatória, oxidativa e redutora na progressão do diabetes melito tipo 1 (DM1) em pacientes sem complicações crônicas. Sujeitos e métodos: Capacidade antioxidante do plasma, espécies reativas de oxigênio (ROS) e interleucina-6 (IL-6) foram avaliadas em 42 pacientes com DM1 e 24 indivíduos saudáveis. Resultados: Aumentos significativos foram detectados nas medianas de ROS e IL-6 em pacientes com DM1 comparados com indiví-duos saudáveis (ROS ~ 4.836 vs. 2.036 RLU/min, respectivamente, P < 0,05: IL-6 ~ 14,2 vs. 9,7 pg/ mL, respectivamente, P = 0,002). Diferenças não significativas (P > 0,05) foram observadas na resposta oxidante e IL-6 quando os diabéticos foram agrupados de acordo com o tempo após o diagnóstico (0-10, 10-20 e > 20 anos). A resposta antioxidante do plasma foi semelhante em pacientes com DM1 e em indivíduos saudáveis. Conclusões: Nossos resultados demonstram que as respostas oxidante e inflamatória estão aumentadas desde o início do DM1, mas mantêm-se inalteradas durante a progressão da doença, sugerindo que as mudanças funcionais envolvidas nas complicações diabéticas podem começar nos primeiros anos após o diagnóstico. Arq Bras Endocrinol Metab. 2012;56(7):441-8 Descritores Diabetes tipo 1; progressão da doença; estresse oxidativo; capacidade oxidante do plasma

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Metabolic Control May Influence the Increased Superoxide Generation in Diabetic Serum

Cited by 106 publications

References 12 publications

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

Early and intermediate Amadori glycosylation adducts, oxidative stress, and endothelial dysfunction in the streptozotocin-induced diabetic rats vasculature

Oxidative stress and interleukin-6 secretion during the progression of type 1 diabetes

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