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Inhibition of the facilitative sugar transporters (GLUTs) by tea extracts and catechins

Research output: Contribution to journalArticlepeer-review

Dejiang Ni, Zeyi Ai, Diana Munoz-Sandoval, Reshma Suresh, Peter R Ellis, Chen Yuqiong, Paul A Sharp, Peter J Butterworth, Zhi Yu, Christopher P Corpe

Original languageEnglish
Pages (from-to)9995-10010
Number of pages16
JournalFaseb Journal
Volume34
Issue number8
Early online date21 Jun 2020
DOIs
Accepted/In press1 Jan 2020
E-pub ahead of print21 Jun 2020
Published1 Aug 2020

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© 2020 Federation of American Societies for Experimental Biology.

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Abstract

Tea polyphenolics have been suggested to possess blood glucose lowering properties by inhibiting sugar transporters in the small intestine and improving insulin sensitivity. In this report, we studied the effects of teas and tea catechins on the small intestinal sugar transporters, SGLT1 and GLUTs (GLUT1, 2 and 5). Green tea extract (GT), oolong tea extract (OT), and black tea extract (BT) inhibited glucose uptake into the intestinal Caco-2 cells with GT being the most potent inhibitor (IC50 : 0.077 mg/mL), followed by OT (IC50 : 0.136 mg/mL) and BT (IC50 : 0.56 mg/mL). GT and OT inhibition of glucose uptake was partial non-competitive, with an inhibitor constant (Ki ) = 0.0317 and 0.0571 mg/mL, respectively, whereas BT was pure non-competitive, Ki = 0.36 mg/mL. Oocytes injected to express small intestinal GLUTs were inhibited by teas, but SGLT1 was not. Furthermore, catechins present in teas were the predominant inhibitor of glucose uptake into Caco-2 cells, and gallated catechins the most potent: CG > ECG > EGCG ≥ GCG when compared to the non-gallated catechins (C, EC, GC, and EGC). In Caco-2 cells, individual tea catechins reduced the SGLT1 gene, but not protein expression levels. In contrast, GLUT2 gene and protein expression levels were reduced after 2 hours exposure to catechins but increased after 24 hours. These in vitro studies suggest teas containing catechins may be useful dietary supplements capable of blunting postprandial glycaemia in humans, including those with or at risk to Type 2 diabetes mellitus.

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