Abstract
Background: The excessive intake of fructose (FRD) induces insulin resistance (IR)-associated renal impairment. Similarly, the use of estrogen-progestin oral contraceptive therapy (EEL) has been associated with cardiometabolic syndrome, and its non-contraceptive benefits particularly in metabolic pathologies remain inconclusive. Therefore, the present study investigated the effects of EEL on renal metabolic function in rats exposed to FRD.Methods: Female rats received vehicle (po), EEL (1.0 µg ethinylestradiol+5.0 µg levonorgestrel.), fructose (10%; w/v) and EEL+FRD respectively for 8 weeks. All data were expressed as means ± SEM and significance were accepted at p<0.05.Results: Data revealed that FRD/EEL caused IR with correspondent increased plasma/renal lipid, decreased glucose-6-dehydrogenase (G6PD), glutathione (GSH) and renal NO/adenosine. FRD but not EEL increased (p<0.05) renal glycogen and decreased (p<0.05) plasma NO/adenosine and pancreatic beta-cell function. These alterations were attenuated when EEL was administered with FRD.Conclusion: The study demonstrates that FRD causes renal impairments accompanied by deficient NO/adenosine concentration and defective G6PD/GSH-dependent antioxidant defense. The findings also suggest that EEL blots the renal effects of FRD.
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