Sarah C Forester1, Yeyi Gu, Joshua D Lambert. 1. Center of Excellence for Plant and Mushroom Foods for Health, Department of Food Science, The Pennsylvania State University, University Park, PA 16802, USA.
Abstract
SCOPE: Green tea has been shown to ameliorate symptoms of metabolic syndrome in vivo. The effects could be due, in part, to modulation of postprandial blood glucose levels. METHODS AND RESULTS: We examined the effect of coadministration of (-)-epigallocatechin-3-gallate (EGCG, 100 mg/kg, i.g.) on blood glucose levels following oral administration of common corn starch (CCS), maltose, sucrose, or glucose to fasted CF-1 mice. We found that cotreatment with EGCG significantly reduced postprandial blood glucose levels after administration of CCS compared to control mice (50 and 20% reduction in peak blood glucose levels and blood glucose area under the curve, respectively). EGCG had no effect on postprandial blood glucose following administration of maltose or glucose, suggesting that EGCG may modulate amylase-mediated starch digestion. In vitro, EGCG noncompetitively inhibited pancreatic amylase activity by 34% at 20 μM. No significant change was induced in the expression of two small intestinal glucose transporters (GLUT2 and SGLT1). CONCLUSIONS: Our results suggest that EGCG acutely reduces postprandial blood glucose levels in mice when coadministered with CCS and this may be due in part to inhibition of α-amylase. The relatively low effective dose of EGCG makes a compelling case for studies in human subjects.
SCOPE: Green tea has been shown to ameliorate symptoms of metabolic syndrome in vivo. The effects could be due, in part, to modulation of postprandial blood glucose levels. METHODS AND RESULTS: We examined the effect of coadministration of (-)-epigallocatechin-3-gallate (EGCG, 100 mg/kg, i.g.) on blood glucose levels following oral administration of common cornstarch (CCS), maltose, sucrose, or glucose to fasted CF-1 mice. We found that cotreatment with EGCG significantly reduced postprandial blood glucose levels after administration of CCS compared to control mice (50 and 20% reduction in peak blood glucose levels and blood glucose area under the curve, respectively). EGCG had no effect on postprandial blood glucose following administration of maltose or glucose, suggesting that EGCG may modulate amylase-mediated starch digestion. In vitro, EGCG noncompetitively inhibited pancreatic amylase activity by 34% at 20 μM. No significant change was induced in the expression of two small intestinal glucose transporters (GLUT2 and SGLT1). CONCLUSIONS: Our results suggest that EGCG acutely reduces postprandial blood glucose levels in mice when coadministered with CCS and this may be due in part to inhibition of α-amylase. The relatively low effective dose of EGCG makes a compelling case for studies in human subjects.
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