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ORIGINAL ARTICLE
Year : 2017  |  Volume : 45  |  Issue : 3  |  Page : 122-128

Role of autophagy and oxidative stress in experimental diabetes in rats


Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt

Correspondence Address:
Asmaa H Okasha
Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Al-Geish Street, Tanta, 31527
Egypt
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DOI: 10.4103/tmj.tmj_2_17

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Background Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia owing to defects in insulin secretion, insulin action, or both. The exact pathogenesis of β-cell failure in type 2 DM is still unclear. However, autophagy and oxidative stress have emerged presently as major contributing factors in the development of type 2 diabetes and β-cell failure. Aim The aim is to assess the levels of beclin-1 (autophagy regulator) and some oxidative stress markers in animal models of high-fat diet-streptozotocin-induced diabetes and to study the effect of 4-phenylbutyrate (4-PBA) on them. Materials and methods The study was conducted on 60 male albino rats that were divided randomly into three equal groups: group I (control group), group II (diabetic group), and group III (diabetic rats treated with 4-PBA). Pancreatic tissue levels of beclin-1 were measured by enzyme-linked immuosorbent assay, whereas pancreatic tissue levels of reduced glutathione (GSH) and plasma levels of advanced oxidation protein products (AOPPs) and glucose were measured spectrophotometrically. Results The levels of beclin-1, AOPPs, and glucose were significantly increased in diabetic group compared with control group, whereas the levels of GSH were significantly decreased. Moreover, 4-PBA significantly decreased the levels of beclin-1, AOPPs, and glucose, whereas it increased GSH levels. Conclusion Autophagy and oxidative stress are involved in the pathogenesis of type 2 DM. Moreover, 4-PBA (a chemical chaperone) attenuated autophagy and exhibited antioxidative stress effects in rats with high-fat diet-streptozotocin-induced diabetes.


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