Abstract
The entrocytes of the small intestine can only absorb monosaccharides such as glucose and fructose from our diet. The intestinal absorption of dietary carbohydrates such as maltose and sucrose is carried out by a group of α-glucosidases. Inhibition of these enzymes can significantly decrease the postprandial increase of blood glucose level after a mixed carbohydrate diet. Therefore, the inhibitory activity of Omija (Schizandra chinensis) extract against rat intestinal α-glucosidase and porcine pancreatic α-amylase were investigated in vitro and in vivo. The in vitro inhibitory activities of water extract of Omija pulp/skin (OPE) on α-glucosidase and α-amylase were potent when compared to Omija seeds extract (OSE). The postprandial blood glucose lowering effect of Omija extracts was compared to a known type 2 diabetes drug (Acarbose), a strong α-glucosidase inhibitor in the Sprague-Dawley (SD) rat model. In rats fed on sucrose, OPE significantly reduced the blood glucose increase after sucrose loading. Furthermore, the oxygen radical absorbance capacity (ORAC) of OSE and OPE was evaluated. OPE had higher peroxyl radical absorbing activity than OSE. These results suggest that Omija, which has high ORAC value with α-glucosidase inhibitory activity and blood glucose lowering effect, could be physiologically useful for treatment of diabetes, although clinical trials are needed.
Highlights
Non-insulin dependent diabetes mellitus (NIDDM, type 2 diabetes) is a common disorder of glucose and fat metabolism that affects 171 million people worldwide, generating immense health care costs [1]
The -amylase inhibitors, which interfere with enzymatic action in the small intestine, could slow the liberation of maltose from starch, resulting in delaying maltose conversion to glucose and decreasing postprandial plasma glucose levels [9]
Insights from this study indicate that Omija skin/pulp extract (OPE) have -glucosidase inhibitory activity and high peroxyl radical scavenging-linked antioxidant activity and have the potential to contribute to the reduction of hyperglycemia-induced microvascular complications
Summary
Non-insulin dependent diabetes mellitus (NIDDM, type 2 diabetes) is a common disorder of glucose and fat metabolism that affects 171 million people worldwide, generating immense health care costs [1]. One of the therapeutic approaches for decreasing postprandial hyperglycemia is to retard digestion of glucose by the inhibition of carbohydrate hydrolyzing enzymes, -amylase and -glucosidase, in the digestive tract [2]. Inhibition of these carbohydrate-hydrolyzing enzymes can significantly decrease the postprandial hyperglycemia after a mixed carbohydrate diet and can be a key strategy in the control of diabetes mellitus [3]. Postprandial hyperglycemia has been linked to the onset of diabetic complications in NIDDM patients and triggers the generation of free radicals and oxidation-related damage in the retina, renal glomerulus and peripheral nerves [4,5]. It is important to control both cellular redox status and blood glucose level for managing these diabetic complications
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
