Abstract
Improvement of oat lines via introgression is an important process for food biochemical functionality. This work aims to evaluate the protective effect of phenolic compounds from hybrid Oat line (F11-5) and its parent (Amlal) on hyperglycemia-induced oxidative stress and to establish the possible mechanisms of antidiabetic activity by digestive enzyme inhibition. Eight phenolic acids were quantified in our samples including ferulic, p-hydroxybenzoic, caffeic, salicylic, syringic, sinapic, p-coumaric and chlorogenic acids. The Oat extract (2000 mg/kg) ameliorated the glucose tolerance, decreased Fasting Blood Glucose (FBG) and oxidative stress markers, including Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Glutathione (GSH) and Malondialdehyde (MDA) in rat liver and kidney. Furthermore, Metformin and Oat intake prevented anxiety, hypercholesterolemia and atherosclerosis in diabetic rats. In vivo anti-hyperglycemic effect of Oat extracts has been confirmed by their inhibitory activities on α-amylase (723.91 μg/mL and 1027.14 μg/mL) and α-glucosidase (1548.12 μg/mL & 1803.52 μg/mL) enzymes by mean of a mixed inhibition.
Highlights
Oxidative stress (OS) has been implicated as a contributor to both the onset and progression of diabetes [1]
In our previous investigation [10], we have described the nutritional characteristics of Moroccan Oat varieties; in this focus the current work aims to compare the therapeutic and preventive effect of a Moroccan hybrid Oat (F11-5) and its parent (Amlal), on oxidative damage and antioxidants enzymes under diabetic status, to evaluate their antioxidant effects in Tetrahymena model, and to characterize the inhibitory properties on digestive enzymes (α-amylase and α-glucosidase)
The dose was selected based on the results of our preliminary oral glucose tolerance tests (OGTTs) assays, in which we found that the effect of the 2000 mg/kg treatment was significantly higher than 500 mg/kg (p < 0.05)
Summary
Oxidative stress (OS) has been implicated as a contributor to both the onset and progression of diabetes [1]. Endogenous reactive oxygen species (ROS) help to maintain homeostasis. The mitochondrial overproduction of ROS in hyperglycemia has been postulated to cause redox imbalance, oxidative insults, mitochondrial dysfunction, and cell death. Many of the common risk factors, such as obesity, increased age, and unhealthy eating habits, enhance pro-oxidative milieu, and may contribute to the development of insulin resistance [4,5], β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction [1], which can lead to the diabetic disease state. Data from experimental and clinical studies suggest an inverse association between insulin sensitivity and radical oxygenated species (ROS) levels [6]. OS contributes in the development of diabetic complications, including diabetic retinopathy, nephropathy, peripheral neuropathy, and cardiovascular disease [7]
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