Effects of Stevioside on oxidative DNA damage in liver and kidney of High Fat Diet Induced type 2 diabetes in Rats

Abstract

Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes and it has been reported to be associated with oxidative stress-induced cellular dysfunction including diabetic nephropathy. Stevioside (STV), a natural non-caloric sweetener refined from the leaves of Stevia rebaudiana Bertoni, has been reported for its insulinotropic and antihyperlipemic effects. In order to investigate the influence of STV on oxidative stress and oxidative DNA damage, high fat-low streptozocin rat model of T2DM were treated orally with 0.125mg/Kg, 0.25mg/Kg and 0.50mg/Kg body weight of STV for 21days. The levels of plasma insulin and dipeptidyl peptidase-4 (DPP IV) were determined using enzyme-linked immunosorbent assay while other biomarkers of T2DM, organ function, oxidative stress and lipid profile were assayed spectrophotometrically. DNA damage in the liver and kidney was determined by assessing the internucleosomal DNA fragmentation pattern on agarose gel electrophoresis. STV treatment resulted in decrease in the levels of fasting plasma glucose, insulin and DPP IV as well as in the activities of plasma amylase and kidney angiotensin-converting enzyme. STV also significantly (p<0.05) improved plasma lipid profile and oxidative stress in the liver and kidney of the diabetic rats, with rats treated with 0.50mg/kg STV having the lowest levels of malondialdehyde and nitric oxide in liver and kidney. There was also a concomitant decrease in the fragmentation of genomic DNA in the liver and kidney of the diabetic rats. This ability of STV, administered orally, to prevent oxidative DNA damage in the liver and kidney of type 2 diabetic rats should contribute to its use in the management of T2DM.