Increased gene expression of antioxidant enzymes in KKAy diabetic mice but not in STZ diabetic mice

Fujita, Atsuyo; Sasaki, Hideyuki; Ogawa, Kenichi; Okamoto, K.; Matsuno, Shohei; Matsumoto, Eisaku; Furuta, Hiroto; Nishi, Masahiro; Nakao, Taisei; Tsuno, Takuo; Taniguchi, Hiroya; Nanjo, Kishio

doi:10.1016/j.diabres.2004.11.016

Cited by 40 publications

(27 citation statements)

References 31 publications

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“…In the present study, this compensatory induction was hindered, probably as a result of rapid and severe hyperglycemia. Similar effects were observed in the kidney of streptozotocin-induced diabetic mice [8] and alloxan-induced diabetic rats [14].…”

Section: Discussionsupporting

confidence: 66%

“…In addition, some authors have described significant hyperglycemia-induced increases in SOD activity [15][16][17]. However, the results have differed and some controversy still exists [8,12,14]. In the present study, this compensatory induction was hindered, probably as a result of rapid and severe hyperglycemia.…”

Section: Discussionmentioning

confidence: 44%

“…So far, increases in the level of 8-OHdG have been reported in mononuclear cells or leukocytes from patients with type 1 and type 2 diabetes mellitus [3,4] and in different tissues from diabetic animals [1,[5][6][7]. High levels of urinary 8-OHdG have also been reported in diabetic patients and animals [2,8,9]. Therefore, the first aim of the present study was to investigate whether hyperglycemia could induce DNA oxidative damage in the kidney of diabetic rabbits.…”

Section: Introductionmentioning

confidence: 99%

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DNA oxidation and superoxide dismutase in the kidney of diabetic animals: effects of pioglitazone and repaglinide

et al. 2006

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Abstract:In the present study, DNA oxidative damage was elevated and superoxide dismutase (Cu,Zn-SOD) metabolism was disturbed in the kidney of alloxan-induced diabetic animals. The effects of pioglitazone and repaglinide, new oral antidiabetics, on 8-hydroxy-2'-deoxyguanosine (8-OHdG) and Cu,Zn-SOD were studied. Diabetic versus control levels (mean ± SE) of 8-OHdG were 24.9 ± 0.2 vs. 21.8 ± 0.1 and 21.5 ± 0.2 vs 20.1 ± 0.2 pmol/µg DNA after 4 and 8 weeks, respectively. At p<0.05, pioglitazone diminished this parameter in diabetic animals (22.0 ± 0.2 and 20.1 ± 0.3 pmol/µg DNA). The level was not affected in diabetic groups receiving repaglinide (24.9 ± 0.2 and 21.5 ± 0.3 pmol/µg DNA). In diabetic kidney, Cu,Zn-SOD mRNA was diminished relative to control animals and was modulated by pioglitazone and repaglinide treatments. Simultaneously, Cu,Zn-SOD activity was also diminished (1.5 ± 0.2 vs. 2.8 ± 0.3 and 1.8 ± 0.1 vs 2.9 ± 0.3 U/mg protein after 4 and 8 weeks, respectively) and partly changed after pioglitazone (2.1 ± 0.4 and 2.3 ± 0.3 U/mg protein) and repaglinide (2.0 ± 0.1 and 2.4 ± 0.2 U/mg protein). These results suggest that a reduction in oxidative stress in diabetic kidney can be achieved with the administration of pioglitazone and to some extent using repaglinide treatment.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 44%

Section: Introductionmentioning

confidence: 99%

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DNA oxidation and superoxide dismutase in the kidney of diabetic animals: effects of pioglitazone and repaglinide

et al. 2006

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“…This apparent discrepancy could be explained by the different obese model (KKAy mice). We carefully checked that the obese rats used in our study are lower insulin sensible but not hyperglycemic, whereas KKAy mice, whatever their age, are obese and hyperglycemic (37). We also demonstrated that adipose tissue of obese organisms shows an active and still adaptable redox metabolism.…”

Section: Discussionmentioning

confidence: 99%

Adipose Tissue Proadipogenic Redox Changes in Obesity

Galinier

Carrière

Fernandez

et al. 2006

Journal of Biological Chemistry

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The role of inflammation and oxidative stress in the development of obesity and associated metabolic disorders is under debate. We investigated the redox metabolism in a non-diabetic obesity model, i.e. 11-week-old obese Zucker rats. Antioxidant enzyme activities, lipophilic antioxidant (␣-tocopherol, coenzymes Q) and hydrophilic antioxidant (glutathione, vitamin C) contents and their redox state (% oxidized form), were studied in inguinal white fat and compared with blood and liver. The adipose tissues of obese animals showed a specific higher content of hydrophilic molecules in a lower redox state than those of lean animals, which were associated with lower lipophilic molecule content and lipid peroxidation. Conversely and as expected, glutathione content decreased and its redox state increased in adipose tissues of rats subjected to lipopolysaccharide-induced systemic oxidative stress. In these in vivo models, oxidative stress and obesity thus had opposite effects on adipose tissue redox state. Moreover, the increase in glutathione content and the decrease of its redox state by antioxidant treatment promoted in vitro the accumulation of triglycerides in preadipocytes. Taken together and contrary to the emergent view, our results suggest that obesity is associated with an intracellular reduced redox state that promotes on its own the development of a deleterious proadipogenic process.Redox metabolism corresponds to a complex interacting network involving the generation of reactive oxygen species and enzymatic and non-enzymatic cellular antioxidant defenses. Any small and transient disturbance of this balance induces redox signaling, which can act on several transduction pathways or enzyme and transcription factor activities. In contrast, when antioxidant defenses are chronically overwhelmed, the result is an oxidative stress in which free radicals may exert their deleterious effects (1). Oxidative stress has been implicated in the pathogenesis of several metabolic diseases as well as in the comorbidity of diabetes mellitus and atherosclerosis. In such studies, redox metabolism was evaluated by the pattern of various parameters such as manganese-dependent superoxide dismutase, glutathione peroxidase or catalase activities, and glutathione or ␣-tocopherol content in blood and liver (2-5). A similar pattern was observed in obesity and seemed to indicate that such pathology was related to pro-oxidative context. Indeed, obesity prevalence is correlated with decreased

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“…Watkins et al (17) reported that there was no difference between the control and diabetic groups during a period of 42 days in terms of the mean body weight of mice. Fujita et al (15) stated a significant decrease in the body weight in STZ diabetic mice compared to the control. Doi et al (14) stated that the body weight of diabetic mice decreased compared to the control mice at the end of a 4-week-long period, and the body weights of the STZ group increased during the study period.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localization of glutathione peroxidase 1 enzyme and its gene expression by RT-PCR in the liver tissue of healthy and diabetic mice

Deprem¹,

Gülmez²

2014

Turk J Vet Anim Sci

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Increased gene expression of antioxidant enzymes in KKAy diabetic mice but not in STZ diabetic mice

Cited by 40 publications

References 31 publications

DNA oxidation and superoxide dismutase in the kidney of diabetic animals: effects of pioglitazone and repaglinide

DNA oxidation and superoxide dismutase in the kidney of diabetic animals: effects of pioglitazone and repaglinide

Adipose Tissue Proadipogenic Redox Changes in Obesity

Immunohistochemical localization of glutathione peroxidase 1 enzyme and its gene expression by RT-PCR in the liver tissue of healthy and diabetic mice

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