Abstract
Chickpeas are an important source of flavonoids in the human diet, and researchers have demonstrated that flavonoids have antidiabetic compositions in chickpeas. Because the NAD+/NADH redox balance is heavily perturbed in diabetes and complex I is the only site for NADH oxidation and NAD+ regeneration, in the present study, mitochondrial complex I was used as a target for anti-diabetes. The objective of this study was to investigate the effects of a crude chickpea flavonoid extract (CCFE) on NAD+/NADH redox imbalance and mitochondrial complex I dysfunction in the pancreas as well as oxidative stress in type 2 diabetes mellitus (T2DM) rats. Our results demonstrated that the degree of NAD+/NADH redox imbalance in the pancreas of T2DM rats was alleviated by CCFE, which is likely attributed to the inhibition of the polyol pathway and the decrease in poly ADP ribose polymerase (PARP) and sirtuin 3 (Sirt3) activities. Moreover, mitochondrial complex I dysfunction in the pancreas of T2DM rats was ameliorated by CCFE through the suppression of the activity of complex I. Furthermore, CCFE treatment could attenuate oxidative stress in T2DM rats, which was proven by the reduction in hydrogen peroxide (H2O2) and malondialdehyde (MDA) as well as the upregulation of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in serum. CCFE treatment significantly improved dyslipidemia in T2DM rats.
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