Abstract
The rice fermented by Monascus, called red mold rice (RMR), and has a long tradition in East Asia as a dietary staple. Monascus-fermented dioscorea called red mold dioscorea (RMD) contains various metabolites to perform the ability of reducing oxidative stress and anti-inflammatory response. We used Wistar rats and induced diabetes by injecting streptozotocin (STZ, 65 mg/kg i.p.). RMD was administered daily starting six weeks after disease onset. Throughout the experimental period, significantly (P < .05) lowered plasma glucose, triglyceride, cholesterol, free fatty acid and low density lipoprotein levels were observed in the RMD-treated groups. The RMD-treated diabetic rats showed higher activities of glutathione disulfide reductase, glutathione reductase, catalase and superoxide dismutase (P < .05) in the pancreas compared with the diabetic control rats. RMD also inhibited diabetes-induced elevation in the levels of interleukin (IL)-1β, IL-6, interferon-γ and tumor necrosis factor-α. Pancreatic β-cells damaged by STZ in the RMD supplemented groups were ameliorated. The results of this study clearly demonstrated that RMD possesses several treatment-oriented properties, including the control of hyperglycemia, antioxidant effects, pancreatic β-cell protection and anti-inflammatory effects. Considering these observations, it appears that RMD may be a useful supplement to delay the development of diabetes and its complications.
Highlights
Diabetes mellitus is a metabolic disease resulting from insulin deficiency, leading to high blood glucose levels and hyperglycemia [1]
[39] The present study shows that red mold dioscorea (RMD) containing a considerable amount of phenolic acid which may be useful in relation to diabetes involving oxidative stress
The results suggest that dioscorea and RMD have beneficial effects on improving the state of a decreased cellular immune function in STZ-induced diabetic rats
Summary
Diabetes mellitus is a metabolic disease resulting from insulin deficiency, leading to high blood glucose levels and hyperglycemia [1]. Hyperglycemia resulting from defection in insulin action or insulin production leads to a number of complications [2]. Diabetic complications have demonstrated that the production of excess reactive oxygen species (ROS) leads to tissue injury or apoptosis [4]. The reduction of antioxidant enzyme activities and tissue glutathione (GSH) levels have been reported in diabetes mellitus [3]. Both oxidative stress and inflammation play a major role in the development of tissue insulin resistance [5]
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