• Journal of Life Science
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• v.27 no.1
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• pp.32-37
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• 2017

Cyanidin-3-O-glucoside (C3G) shows anti-inflammatory and antioxidant effects; however, its effect on postprandial blood glucose levels remains unknown. Alpha-glucosidase inhibitors regulate post-prandial hyperglycemia by impeding carbohydrate digestion in the small intestine. Here, the effect of C3G on ${\alpha}-glucosidase$ and ${\alpha}-amylase$ inhibition and its ability to ameliorate postprandial hyperglycemia in streptozotocin (STZ)-induced diabetic mice were evaluated. ICR normal and STZ-induced diabetic mice were orally administered soluble starch alone or with C3G or acarbose. The half-maximal inhibitory concentrations of C3G for ${\alpha}-glucosidase$ and ${\alpha}-amylase$ were 13.72 and $7.5{\mu}M$, respectively, suggesting that C3G was more effective than acarbose. The increase in postprandial blood glucose levels was more significantly reduced in the C3G groups than in the control group for both diabetic and normal mice. The area under the curve for the diabetic mice was significantly reduced following C3G administration. C3G may be a potent ${\alpha}-glucosidase$ inhibitor and may delay dietary carbohydrate absorption.

• Journal of Nutrition and Health
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• v.44 no.3
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• pp.196-202
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• 2011

Epigallocatechin gallate (EGCG), or epigallocatechin 3-gallate, is the ester of epigallocatechin and gallic acid, and is a type of catechin. EGCG may be therapeutic for many disorders including diabetics and some types of cancer. However it is unknown whether EGCG can induce transdifferentiation of pancreatic cells in pancreatitis. The aim of this study was to investigate the effects of EGCG on the expression of pancreatic regenerating related markers in pancreatic AR42J cells, a model of pancreatic progenitor cells. AR42J cells, differentiated with betacellulin and activin A, were cultured with/without EGCG in a time-dependent manner. Cell growth rate, levels of mRNA, and protein expression were examined with the MTT assay, quantitative PCR, and Western blots, respectively. The results showed that AR42J cell growth rates were inhibited by EGCG in a dose-dependent manner. mRNA and protein expression of amylase, insulin and neurogenin 3 (ngn 3) increased in AR42J cells treated with EGCG. Additionally, we demonstrated that the signal transduction pathway of mitogen-activated protein (MAP) kinase is active in EGCG-treated AR42J cells. ERK and JNK phosphorylation decreased in cells treated with EGCG but not p38 phosphorylation. Activation of the p38 MAP kinase pathway was confirmed by specific MAP kinase pathways inhibitors: U0126 for ERK, SP600126 for JNK, and SB203580 for p38. Activated p38 phosphorylation was inhibited by the specific p38 inhibitor SB203580 but p38 phosphorylation was inhibited with increased EGCG treatment. The ERK and JNK MAP kinase pathways were not affected by EGCG treatment. Although further studies are needed, these results suggest that EGCG affects the induction of pancreatic cell regeneration by increasing the ngn 3 protein and mRNA expression and activating the p38 MAP kinase pathway.

• Journal of Life Science
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• v.26 no.8
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• pp.921-927
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• 2016

Postprandial hyperglycemia is an early defect of type 2 diabetes and one of primary anti-diabetic targets. The alpha-glucosidase inhibitors regulate postprandial hyperglycemia by impeding the rate of carbohydrate (such as starch) digestion in the small intestine. This study was designed to investigate the inhibitory actions of mulberry fruit extract (MFE) on α-glucosidase and α-amylase activities, and its alleviating effect on postprandial hyperglycemia activities in vitro and in vivo. Male four-week old ICR mice and streptozotocin (STZ)-induced diabetic mice were treated with mulberry fruit extract. MFE showed strong inhibitory effects against α-glucosidase and α-amylase activities, with half-maximal inhibitory concentration (IC₅₀) values of 0.16 and 0.14 mg/ml, respectively, and was more effective than acarbose, which was used as a positive control. The increase in postprandial blood glucose levels was more significantly attenuated in the MFE-administered group mice than in the control group mice of both STZ-induced diabetic and normal mice. Moreover, the area under the glucose response curve significantly decreased following MFE administration in diabetic mice. These results indicate that MFE may be a potent inhibitor of α-glucosidase and α-amylase, and helpful in suppressing postprandial hyperglycemia in diabetic mice. The mulberry fruit extracts may be considered as a potential candidate for the management of diabetes.