Exercise Training Prevents and Protects Streptozotocin-Induced Oxidative Stress and .BETA.-Cell Damage in Rat Pancreas

Abstract

The aim of the present study was the evaluation of possible protective effects of exercise against β -cell damage in streptozotocin (STZ)-induced diabetes in rats. The animals were divided into five groups: the control group, the STZ-induced diabetes group, the STZ-induced diabetes and light-intensity exercise group, the STZ-induced diabetes and moderate-intensity exercise group, and the STZ-induced diabetes and heavyintensity exercise group. Animals in the exercise groups were made to swim one of three exercise protocols once a day for 12 consecutive weeks. STZ was injected intraperitoneally at a single dose of 50 mg/kg for diabetes induction. Exercise training was continued for 4 weeks prior to STZ administration; these applications were continued end of the study (for 12 weeks). Erythrocyte and pancreatic tissue malondialdehyde (MDA) levels and serum nitric oxide (NO) concentration were measured. Moreover glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) were also measured in pancreatic homogenates. Pancreatic β -cells were examined by immunohistochemical methods. STZ increased lipid peroxidation and decreased the antioxidant enzyme activity significantly. Exercise, especially moderate-intensity exercise has shown protective effect probably through decreasing lipid peroxidation and increasing antioxidant enzyme activity. Islet cell degeneration and weak insulin immunohistochemical staining were observed in STZ induced diabetic rats. Increased intensity of staining for insulin and preservation of β -cell numbers were apparent in the exercise-applied diabetic rats. Interestingly, the best result was obtained from moderate-intensity exercise. These findings suggest that exercise has a therapeutic and/or protective effect in diabetes by decreasing oxidative stress and preservation of pancreatic β -cell integrity.exercise; diabetes; streptozotocin; β -cell; oxidative stress

Nuclear Factor-.KAPPA.B Activation in Diabetic Rat Kidney: Evidence for Involvement of P-Selectin in Diabetic Nephropathy

“…The present study has shown the involvement of P-selectin in the development of DN through NF-κ B activation in the renal cortex of STZ-treated rats, an animal model of DN (Portha et al 1979(Portha et al , 1989Coskun et al 2004). This finding is consistent with previous observations of increased P-selectin expression in kidneys of patients with DN (Hirata et al 1998) and of upregulated human P-selectin gene expression due to NF-κ B activation (Pan and McEver 1995;Weyrich et al 1995).…”

“…In this study, we investigated the activation of NF-κ B focusing on P-selectin expression in the renal cortex of streptozotocin (STZ)-treated rats, a widely utilizing animal model of diabetes mellitus (Portha et al 1979(Portha et al , 1989Coskun et al 2004). Our results demonstrate that P-selectin may be involved in the onset and progression of DN through NF-κ B activation.…”

The time has come to test the beta cell preserving effects of exercise in patients with new onset type 1 diabetes

“…One is to ablate beta cells using a beta cell toxic agent such as streptozotocin (STZ). When initiated 4 weeks prior to STZ treatment in rats, exercise training preserved beta cell number and increased beta cell insulin content [32]. Furthermore in a study by Huang et al, while exercise did not improve islet diameter or beta cell mass, islet insulin content and insulin secretion was greater in exercised vs sedentary STZ-induced diabetic mice [33].…”

Ameliorative effects of aminoguanidine on rat aorta in Streptozotocin-induced diabetes and evaluation of α-SMA expression

“…Many actions have been attributed to STZ that are including damage to the pancreatic β-cell membrane and decreases insulin secretion from the β-cell. In addition, STZ has been shown to induce DNA strand breaks and methylation in pancreatic islet cells (9,11,12).…”