Gliclazide protects pancreatic β-cells from damage by hydrogen peroxide

Kimoto, Kiyoko; Suzuki, Kenji; Kizaki, Takako; Hitomi, Yoshiaki; Ishida, Hideyuki; Katsuta, Hidenori; Itoh, Eriko; Ookawara, Tomomi; Suzuki, Keiichiro; Honke, Koichi; Ohno, Hideki

doi:10.1016/s0006-291x(03)00310-3

Cited by 81 publications

(35 citation statements)

References 36 publications

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“…Other studies question these deleterious effects of sulfonylureas. It has previously been reported that tolbutamide stimulates β cell proliferation from neonatal rats in a Ca 2+ -dependent manner (53) and that gliclazide protects insulin-secreting MIN6 cells from H 2 O 2 -induced damage (54), which is consistent with our present data. Another study reports that chronic glibenclamide treatment reduces glucose-induced insulin secretion in mice and induces diabetes (55).…”

Section: Discussionsupporting

confidence: 93%

“…This difference from tolbutamide may be due to the fact that gliclazide additionally acts as a free radical scavenger (68). Beneficial effects of gliclazide on survival of primary β cell and insulin-secreting cell lines have been reported in several recent papers (54,69,70). Administration of gliclazide represents a strategy to lower blood glucose concentration and additionally to delay diabetic complications such as micro-and macroangiopathies (71)(72)(73).…”

Section: Figurementioning

confidence: 99%

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Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

et al. 2009

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The enhanced oxidative stress associated with type 2 diabetes mellitus contributes to disease pathogenesis. We previously identified plasma membrane-associated ATP-sensitive K + (K ATP ) channels of pancreatic β cells as targets for oxidants. Here, we examined the effects of genetic and pharmacologic ablation of K ATP channels on loss of mouse β cell function and viability following oxidative stress. Using mice lacking the sulfonylurea receptor type 1 (Sur1) subunit of K ATP channels, we found that, compared with insulin secretion by WT islets, insulin secretion by Sur1 -/-islets was less susceptible to oxidative stress induced by the oxidant H 2 O 2 . This was likely, at least in part, a result of the reduced ability of H 2 O 2 to hyperpolarize plasma membrane potential and reduce cytosolic free Ca 2+ concentration ([Ca 2+ ] c ) in the Sur1 -/-β cells. Remarkably, Sur1 -/-β cells were less prone to apoptosis induced by H 2 O 2 or an NO donor than WT β cells, despite an enhanced basal rate of apoptosis. This protective effect was attributed to upregulation of the antioxidant enzymes SOD, glutathione peroxidase, and catalase. Upregulation of antioxidant enzymes and reduced sensitivity of Sur1 -/-cells to H 2 O 2 -induced apoptosis were mimicked by treatment with the sulfonylureas tolbutamide and gliclazide. Enzyme upregulation and protection against oxidant-induced apoptosis were abrogated by agents lowering [Ca 2+ ] c . Sur1 -/-mice were less susceptible than WT mice to streptozotocin-induced β cell destruction and subsequent hyperglycemia and death, which suggests that loss of K ATP channel activity may protect against streptozotocin-induced diabetes in vivo.

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Section: Discussionsupporting

confidence: 93%

Section: Figurementioning

confidence: 99%

Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

et al. 2009

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“…Other successful attempts to ameliorate diabetes and oxidative stress in animal models have involved the use of vitamin E in Goto-Kakizaki rats [65] and gliclazide [66], an oral hypoglycemic agent with antioxidant properties. Zucker diabetic fatty (ZDF) rats carry a mutation in the leptin receptor gene and become obese and diabetic with age.…”

Section: Antioxidative Therapy In Animal Studiesmentioning

confidence: 99%

Oxidative Stress, Nitric Oxide, and Diabetes

Pitocco¹,

Zaccardi²,

Stasio³

et al. 2010

Rev Diabet Stud

288

194

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■ AbstractIn the recent decades, oxidative stress has become focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence from research on several diseases show that oxidative stress is associated with the pathogenesis of diabetes, obesity, cancer, ageing, inflammation, neurodegenerative disorders, hypertension, apoptosis, cardiovascular diseases, and heart failure. Based on this research, the emerging concept is that oxidative stress is the "final common pathway", through which risk factors of several diseases exert their deleterious effects. Oxidative stress causes a complex dysregulation of cell metabolism and cell-cell homeostasis. In this review, we discuss the role of oxidative stress in the pathogenesis of insulin resistance and beta-cell dysfunction. These are the two most relevant mechanisms in the pathophysiology of type 2 diabetes, and in the pathogenesis of diabetic vascular complications, the leading cause of death in diabetic patients.

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“…However, the action of repaglinide and sulfonylureas on Cu,Zn-SOD expression has been examined poorly so far. In one previous study, Cu,Zn-SOD mRNA was elevated by gliclazide in pancreatic beta cells treated with H 2 O 2 [30].…”

Section: Discussionmentioning

confidence: 77%

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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Gliclazide protects pancreatic β-cells from damage by hydrogen peroxide

Cited by 81 publications

References 36 publications

Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

Oxidative Stress, Nitric Oxide, and Diabetes

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

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